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A/I Board Review > Abbas > Flashcards

Abbas Flashcards

1
Q

How many neutrophils are produced in an adult in any given day?

A

1x10^11

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2
Q

Classical monocytes are identified by which three surface markers?

A

High cell surface expression of CD14
Lack of expression of CD16
Expression of the chemokine receptor CCR2

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3
Q

What is the function of classical monocytes and where are they found?

A

Classical or inflammatory monocytes produce inflammatory mediators, are phagocytic, and are rapidly recruited to sites of infection or tissue injury. These cells also are found in the spleen, from where they can be recruited into the circulation in response to systemic inflammatory stimuli. In humans, classical (inflammatory) monocytes are identifiable by high cell surface expression of CD14, lack of expression of CD16, and expression of the chemokine receptor CCR2

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4
Q

What is the function of nonclassical monocytes?

A

Nonclassical monocytes, are recruited into tissues after infection or injury and may contribute to repair. Some of these cells are known to crawl along endothelial surfaces (described as patrolling). In humans, nonclassical monocytes make up a minority of blood monocytes and are identified by low levels of CD14 and high levels of CD16 and the chemokine receptor CX3CR1

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5
Q

Nonclassical monocytes are identified by which three surface markers?

A

Low levels of CD14
High levels of CD16
Expression of the chemokine receptor CX3CR1

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6
Q

Cytokines are essential for the survival of naive lymphocytes, and naive B and T cells express receptors for these cytokines. The most important of these cytokines are ____, which promotes survival and low-level cycling of naive T cells, and ______, which is required for naive B cell survival.

A

Cytokines are also essential for the survival of naive lymphocytes, and naive B and T cells express receptors for these cytokines. The most important of these cytokines are IL-7, which promotes survival and low-level cycling of naive T cells, and B cell–activating factor (BAFF), a cytokine belonging to the tumor necrosis factor (TNF) family, which is required for naive B cell survival.

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7
Q

What is the surface protein expression levels for naive T cells vs effector/activated T cells vs memory T cells?

  • IL-2R (CD25)
  • L-selectin (CD62L)
  • IL-7R (CD127)
  • CCR7
A

Naive / Activated / Memory

  • IL-2R Low / High / Low
  • L-selectin High / Low / Variable
  • IL-7R High / Low / High
  • CCR7 High / Low / Variable
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8
Q

What is the major CD45 isoform expressed by naive T cells vs effector/activated T cells vs memory T cells?

A

Naive: CD45RA
Effector: CD45RO
Memory: CD45RO; variable

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9
Q

What are the main transcription factors for Th1?

A

Th1 – T-bet, STAT1, STAT4

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10
Q

What are the main transcription factors for Th2?

A

Th2 – GATA-3, STAT 6

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11
Q

What are the main transcription factors for Th17?

A

Th17 – RORγT

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12
Q

What are the main transcription factors for Treg?

A

Treg – STAT5

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13
Q

During fetal life, which cells stimulate the development of lymph nodes and other secondary lymphoid organs?

A

During fetal life, lymphoid tissue–inducer cells, which are a subset of ILCs, stimulate the development of lymph nodes and other secondary lymphoid organs. This function is mediated by various proteins expressed by the inducer cells, the most thoroughly studied being the cytokines lymphotoxin-α (LTα) and lymphotoxin-β (LTβ). Knockout mice lacking either of these cytokines do not develop lymph nodes or secondary lymphoid tissues in the gut. Splenic white pulp development is also disorganized in these mice. LTβ produced by the inducer cells stimulates stromal cells in different locations of a developing secondary lymphoid organ to secrete chemokines that help to organize the structure of the lymphoid organs.

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14
Q

FDCs are activated by LTβ to produce the chemokine(s) ____ which serves to recruit naive B cells. What is the B cell receptor?

A

The chemokine CXCL13 and its receptor CXCR5 on B cells are required for B cell migration into the follicles. Table also includes CXCL12 and CXCR4.

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15
Q

FDCs are activated by LTβ to produce the chemokine(s) _________ which recruit naive T cells. What is the T cell receptor?

A

The chemokines CCL19 and CCL21 and their receptor CCR7 on T cells are required for naive T cell migration

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16
Q

FDCs are activated by LTβ to produce the chemokine(s) _________ which recruit DCs. What is the DC receptor?

A

CCL19 and CCL21. DCs express CCR7, and this explains how DCs and naive T cells localize to the same place in lymph nodes, enabling the DCs to present antigen to the T cells.

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17
Q

What is the distribution and ligand for P-selectin?

A 
Distribution = endothelium activated by histamine or thrombin
Ligand = Sialyl Lewix X; neutrophils, monocytes, T cells
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18
Q

What is the distribution and ligand for E-selectin?

A 
Distribution = endothelium activated by cytokines (TNF, IL-1)
Ligand = Sialyl Lewis X; neutrophils monocytes, T cells
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19
Q

What is the distribution and ligand for L-selectin?

A 
Distribution = neutrophils, monocytes, T cells, B cells
Ligand = Sialyl Lews X, CD34, MadCAM-1; endothelium (HEV)
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20
Q

What is the distribution and ligand for LFA-1?

A 
Distribution = neutrophils, monocytes, T cells, B cells
Ligand = ICAM-1, ICAM-2; endothelium (upregulated when cytokine activated)
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21
Q

What is the distribution and ligand for Mac-1?

A 
Distribution = Neutrophils, monocytes, DCs
Ligand =  ICAM-1, ICAM-2; endothelium (upregulated when cytokine activated)
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22
Q

What is the distribution and ligand for VLA-4?

A 
Distribution = monocytes, T cells
Ligand =  VCAM-1; endothelium (upregulated when cytokine activated)
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23
Q

What is the distribution and ligand for A4B7?

A 
Distribution = Monocytes, T cells (gut-homing), B cells (gut-homing)
Ligand =  VCAM-1, MadCAM-1; endothelium  in gut and gut-associated lymphoid tissues
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24
Q

What two types of selectins are expressed by endothelial cells?

A

P-selectin and E-selectin
P-selectin, so named because it was first found in platelets, is stored in cytoplasmic granules of endothelial cells and is rapidly redistributed to the luminal surface in response to histamine from mast cells and thrombin generated during blood coagulation. E-selectin is synthesized and expressed on the endothelial cell surface within 1 to 2 hours in response to the cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF), which are produced by tissue sentinel cells (DCs and macrophages) in response to infection. Microbial products such as lipopolysaccharide (LPS) also stimulate E-selectin expression on endothelial cells.

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25
Q

What is the defect for each type of leukocyte adhesion deficiency?
LAD-1
LAD-2
LAD-3

A

LAD-1 – AR deficiency in the CD18 gene which encodes the B subunit of LFA-1 and Mac-1
LAD-2 – lack Golgi GDP-fucose transported needed to express E-selectin and P-selectin
LAD-3 – mutation in signaling pathways linking chemokine receptors to integrin activation

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26
Q

What is the clinical presentation for leukocyte adhesion deficiencies?

A

Recurrent bacterial and fungal infections, lack of neutrophil accumulation at sites of infection, defects in adherance-depedent lymphocyte functions

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27
Q

What chemokine-chemokine receptor pairs are involved in neutrophil recruitment into tissues?

A

CXCL1 - CXCR2

CXCL8 - CXCR1, CXCR2

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28
Q

What chemokine and chemokine receptor pair is the HIV coreceptor?

A

CCL4-CCR5

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29
Q

Where is S1P present in high concentrations? What about S1PR1?

A

S1P is present at higher concentrations in the blood and lymph than in tissues. This concentration gradient is maintained because an S1P-degrading enzyme, S1P lyase, is present in most tissues, so the lipid is catabolized in tissues more than in the lymph and blood. S1PR1 stimulates migration of cells towards a gradient of S1P.

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30
Q

Describe how S1P and S1PR1 help with naive T cell circulation.

A

Circulating naive T cells have very little surface S1PR1 because the high blood concentration of S1P causes internalization of the receptor. After a naive T cell enters a lymph node, where S1P concentrations are low, S1PR1 reappears on the cell surface over a period of several hours. This time lag allows a naive T cell to interact with antigen-presenting cells. After the S1PR1 receptor is expressed, the T cell leaves the lymph node and is directed down the S1P concentration gradient into the efferent lymphatic.

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31
Q

Describe how S1P and S1PR1 help with activated T cell circulation

A

If a naive T cell is activated by antigen in the lymph node, the surface expression of S1PR1 is suppressed for several days, and therefore, the ability of the cells to leave the lymphoid organ in response to an S1P gradient is delayed. This suppression of S1PR1 is controlled in part by cytokines called type I interferons that are produced during innate immune responses to infections, as we will discuss in Chapter 4. Antigenic stimulation and interferons together increase the expression of a protein called CD69, which binds to intracellular S1PR1 and reduces its cell surface expression. Thus, the activated T cell becomes transiently insensitive to the S1P gradient. This allows the antigen-activated T cells to remain in the lymphoid organ and undergo clonal expansion and differentiation into effector T cells, a process that may take several days. When differentiation into effector cells is complete, the cells lose CD69, and S1PR1 is again expressed on the cell surface. Therefore, the effector T cells become responsive to the concentration gradient of S1P and exit the lymph node via the medullary sinus draining into the efferent lymphatic.

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32
Q

Which TLRs are located on the plasma membrane?

A

TLR1:TLR2, TLR2, TLR4, TLR5, TLR2:TLR6

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33
Q

Which TLRs are located on endosomal membranes?

A

TLR3, TLR7, TLR8, TLR9

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34
Q

What does TLR1:TLR2 recognize? Where is it located?

A

Bacterial lipoproteins. Plasma membrane

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35
Q

What does TLR2 recognize? Where is it located?

A

Bacterial peptidoglycan. Plasma membrane

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36
Q

What does TLR4 recognize? Where is it located?

A

LPS. Plasma membrane

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37
Q

What does TLR5 recognize? Where is it located?

A

Bacterial flagellin. Plasma membrane

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38
Q

What does TLR2:TLR6 recognize? Where is it located?

A

Bacterial lipopeptides. Plasma membrane

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39
Q

What does TLR3 recognize? Where is it located?

A

dsRNA. Endosome

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40
Q

What does TLR7 recognize? Where is it located?

A

ssRNA. Endosome

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41
Q

What does TLR8 recognize? Where is it located?

A

ssRNA. Endosome

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42
Q

What does TLR9 recognize? Where is it located?

A

CpG DNA. Endosome

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43
Q

Which TLRs signal through MyD88? Which signal through TRIF? Which signal through both?

A

TLR1, TLR2, TLR5, TLR6, TLR7, TLR9 signal through MyD88
TLR4 signals through MyD88 and TRIF
TLR3 signals through TRIF

MyD88 and TRIF signal through NF-kB causing acute inflammation and IRFs which causes secretion of type 1 IFNs responsible for the antiviral state

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44
Q

Antiallotypic antibodies are formed against what part of the antibody?

A

The C regions of Ig heavy and light chains. Polymorphic variants in these regions are called allotypes.

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45
Q

Anti-idiotypic antibodies are formed against what part of the antibody?

A

The CDRs of the V regions.

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46
Q

What is the difference between a conformational determinant, linear determinant, and neodeterminants?

A

Conformational - determinant lost by denaturation
Linear - Ig binds to determinant in denatured protein only or Ig binds to determinant in both native and denatured protein
Neodeterminant - Arise from postsynthetic modifications such as peptide bone cleavage

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47
Q 
How long is the half-life of each of the following in circulation?
IgE
IgA
IgM
IgG
A

IgE – 2 days (cell-bound IgE associated with high-affinity IgE receptor on mast cells has a very long half life)
IgA – 3 days
IgM – 4 days
IgG 21-28 days

48
Q

Why is the IgG half-life so much longer than other antibodies?

A

The long half-life of IgG is attributed to its ability to bind to a specific Fc receptor called the neonatal Fc receptor (FcRn). FcRn structurally resembles MHC class I molecules. It is found on the surface of endothelial cells, macrophages, and other cell types, and binds to micropinocytosed IgG in acidic endosomes. FcRn does not target bound IgG to lysosomes (the usual fate of many ingested molecules) but recycles it to the cell surface and releases it at neutral pH, returning the IgG to the circulation. This intracellular sequestration of IgG away from lysosomes prevents the IgG from being degraded as rapidly as most other plasma proteins, including other antibody isotypes, and as a result, this antibody isotype has a relatively long half-life. There are some differences in the half-lives of the four human IgG isotypes. IgG3 is relatively short-lived because it binds poorly to FcRn. IgG1 and IgG2 are the most long-lived and most efficient in terms of effector functions, as will be discussed in Chapter 13.

49
Q

Features of Class II MHC

  • polypeptide chains
  • locations of polymorphic residues
  • Binding site for T cell coreceptor
  • Size of peptide-binding cleft
  • Nomenclature
A
  • polypeptide chains = alpha and beta
  • locations of polymorphic residues = a1 and B1
  • Binding site for T cell coreceptor = CD4 binds to a pocket created by parts of a2 and B2
  • Size of peptide-binding cleft = 10-30 amino acids or more
  • Nomenclature = HLA-DR, HLA-DQ, HLA-DP
50
Q

Features of Class I MHC

  • polypeptide chains
  • locations of polymorphic residues
  • Binding site for T cell coreceptor
  • Size of peptide-binding cleft
  • Nomenclature
A
  • polypeptide chains = alpha and beta2-microglobulin
  • locations of polymorphic residues = a1 and a2
  • Binding site for T cell coreceptor = CD8 binds mainly to the a3 domain
  • Size of peptide-binding cleft = 8-11 amino acids
  • Nomenclature = HLA-A, HLA-B, HLA-C
51
Q

NK cells recognize antigens presented by ______

A

CD-1

52
Q

What causes bare lymphocyte syndrome

A

CIITA functions as a master regulator of class II gene expression. Mutations in CIITA or the associated transcription factors have been identified as the cause of human immunodeficiency diseases associated with defective expression of MHC molecules. The best studied of these disorders is bare lymphocyte syndrome

53
Q

What is the major difference between non-receptor tyrosine kinase based receptors and tyrosine kinase receptors?

A

Non-receptor tyrosine kinase based receptors lack intrinsic catalytic activity.

54
Q

When TCR engages its ligand, which signaling molecules are directly activated?

A

CD3 and zeta chain of TCR

  • The CD3 proteins and the ζ chain are identical in all T cells regardless of specificity, which is consistent with their role in signaling and not in antigen recognition.
  • Ligation of the TCR by MHC-peptide ligands results in the clustering of coreceptors with the antigen receptor and phosphorylation of ITAM tyrosine residues in CD3 and ζ proteins. In addition, recognition of peptide-MHC complexes by the TCR may induce a conformational change in the TCR, making the ITAMs associated with the linked CD3 or ζ chains available for tyrosine phosphorylation by Src family kinases.
55
Q

What is the ligand-receptor pair for each of the following surface molecules involved in T cell activation/inhibition? What is the function of the surface molecule?

  • CD4
  • CD8
  • CD28
  • CTLA-4
  • PD-1
  • LFA-1
A
  • CD4 - signal transduction – Class II MHC
  • CD8 - signal transduction – Class I MHC
  • CD28 - signal transduction (co-stimulation) – B7-1/B7-2
  • CTLA-4 - inhibition – B7-1/B7-2
  • PD-1 - inhibition – PD-L1/PD-L2
  • LFA-1 - adhesion – ICAM-1
56
Q

On which cell types are class II MHC expressed? What about class I MHC?

A

MHC II – APCs

MHC I – all nucleated cells

57
Q

Which transcription factors commit developing lymphocytes to the T cell lineage?

A

The Notch-1 and GATA-3 transcription factors commit developing lymphocytes to the T cell lineage.

58
Q

Which transcription factors commit developing lymphocytes to the B cell lineage?

A

The EBF, E2A, and Pax-5 transcription factors induce the expression of genes required for B cell development.

59
Q

Mutation in what gene gives rise to X-liked SCID?

A

Mutations in the gene for the common γ chain, a protein that is shared by the receptors for several cytokines, including IL-2, IL-7, and IL-15 among others, give rise to an immunodeficiency disorder in humans called X-linked severe combined immunodeficiency disease (X-SCID). This disease is characterized by a block in T cell and NK cell development, but normal B cell development, reflecting the requirement for IL-7 in T cell development in humans and of IL-15 for NK cells.

60
Q

What happens if Dicer is deleted?

A

Dicer is a key enzyme in miRNA generation. Deletion of Dicer in the T lineage results in a preferential loss of regulatory T cells and the consequent development of an autoimmune phenotype similar to that seen in the absence of FoxP3. The loss of Dicer in the B lineage results in a block at the pro-B to pre-B cell transition, primarily by being permissive for the apoptosis of pre-B cells.

61
Q

Entry of T cell precursors into the thymus is dependent on ___ binding the chemokine ligand ____, which is produced in the thymic cortex.

A

Entry of these precursors into the thymus is dependent on CCR9 binding the chemokine ligand CCL25, which is produced in the thymic cortex. Chemokines such as CCL21 and CCL19, which bind to the CCR7 chemokine receptor on thymocytes, direct the movement of developing T cells from the cortex to the medulla. Eventually, newly formed T lymphocytes, which express the sphingosine 1-phosphate receptor (see Chapter 3), exit the thymic medulla following a gradient of sphingosine-1 phosphate into the blood stream.

62
Q

What are the different causes of hyper-IgM syndrome?

A
  1. X-linked – mutation in CD40L – Defects in T helper cell–mediated B cell, macrophage, and dendritic cell activation; defects in somatic mutation, class switching, and germinal center formation; defective cell-mediated immunity
  2. AR with cell-mediated immune defects – mutations in CD40, NEMO – Defects in T helper cell–mediated B cell, macrophage, and dendritic cell activation; defects in somatic mutation, class switching, and germinal center formation; defective cell-mediated immunity
  3. AR with antibody defect only – mutations in AID, UNG – Defects in somatic mutation and isotype switching
63
Q 
Which of the following cell types is a phagocyte?
Plasma cell
Neutrophil
Mast cell
Natural killer cell
T lymphocyte
A

Neutrophils (and macrophages) are the major phagocytes in the immune system, and function to internalize and kill microbes. Phagocytes also internalize and break down dead cells and nonmicrobial foreign materials. The other cell types listed have minimal phagocytic capabilities.

64
Q 
Migration of leukocytes out of the blood into tissues mainly occurs in which type of vessel?
Arteries
Arterioles
Capillaries
Venules
Veins
A

All leukocytes mainly migrate into tissues through the walls of post capillary venules, because the flow characteristics in venules favor leukocyte endothelial interactions, and the endothelial cells lining post capillary venules are specialized to express adhesion molecules required for leukocyte interactions with endothelial cells, and to produce and display chemokines that promote binding to endothelium and migration of the leukocytes.

65
Q

Which of the following accurately describe the function of the selectin family of adhesion molecules?

  • Selectins support low affinity rolling of leukocytes on endothelial cells
  • Endothelial selectins increase their affinity for binding to leukocytes in response to chemokines
  • Selectins guide migration of leukocytes though interendothelial junctions
  • Selectins are expressed only on naïve T cells
  • Selectins play a direct role in clonal selection
A

E-selectin and P-selectin expressed on cytokine-activated endothelial cells bind weakly to carbohydrate ligands expressed on various leukocytes including lymphocytes, monocytes, and granulocytes. The fluid shear force caused by the flow of blood causes the selectin-selectin ligand bonds to break and then reform as the cells are pushed along; the net result is rolling of the leukocytes along the endothelial surface. Rolling interactions are also mediated by L-selectin on some leukocytes binding to their carbohydrate ligand on the endothelium.

66
Q

Which of the following is one of the major functions of chemokines in the immune system?
A) Increase affinity of leukocyte selectins for their ligands on endothelial cells.
B) Stimulate proliferation of B cells in response to antigen
C) Increase vascular permeability during the innate immune response to microbes
D) Maintain the spatial separation of B and T lymphocytes within lymphoid tissues
E) Form pores in bacterial membranes

A

D – Chemokines have three major functions in the immune system. 1. Chemokines activate leukocytes to increase integrin affinity, which is needed for stable arrest of leukocytes on endothelial cells before they can migrate into tissues 2. Chemokines promote movement of leukocytes towards the source of the chemokines such as an infected phagocyte. 3. Distinct chemokines that are continually produced in follicles or interfollicular regions of lymphoid tissues maintain the location of B cells in the follicles and T cells outside the follicles.

67
Q

Which of the following statements correctly describes the migratory behavior of naïve T lymphocytes?

  • They recirculate from blood into lymph nodes via high endothelial venules, and back into blood via lymphatics
  • They recirculate from blood into inflamed tissues via activated post capillary venules, and back into blood via lymphatics
  • They migrate into the thymus via high endothelial venules, where they mature into effector T cells, which then enter the blood via lymphatics
  • They are stationary within lymph nodes and do not migrate
  • After maturation in the thymus, they migrate into the blood via draining lymphatics and enter the spleen via high endothelial venules
A

Naïve T cells enter lymph nodes via high endothelial venules, a process dependent on the chemokine receptor CCR7 and L-selectin on the naïve T cells. If after several hours the naive T cell is not activated by antigen, it will exit the lymph node via efferent lymphatics, and flow via lymph channels back into the blood. Naïve T cells do not migrate into peripheral sites of inflammation, and although they are formed in the thymus, they do not exit via lymphatics but rather via blood vessels. Migration of naïve T cells into spleen is not via high endothelial venules (which are not present in the spleen).

68
Q

Fingolimod is a drug used to treat autoimmune disease, which blocks the function of sphingosine-1 phosphate (S1P) by binding to its receptor S1PR1. Patients treated with fingolimod become lymphopenic, i.e. they have low numbers of lymphocytes in the blood. Why?

  • S1P binding to S1PR1 is required for T cell maturation in the thymus
  • S1P binding to S1PR1 stimulates lymphocyte clonal expansion
  • S1P binding to S1PR1 blocks lymphocyte migration out of the blood into lymph nodes
  • S1P binding to S1PR1 inhibits lymphocyte apoptosis
  • S1P binding to S1PR1 on lymphocytes is required for exit of lymphocytes from lymphoid tissues
A

The exit of naive T cells from lymph nodes and thymus requires the lipid chemoattractant S1P, which binds to S1PR1 on T cells. S1P is present at high concentrations in the blood and lymph compared with lymphoid tissues. Naive T cells in the blood have little surface S1PR1 because the high blood concentration of S1P causes receptor down regulation. When a naive T cell enters a lymph node, it takes several hours for the surface S1P1R to be re-expressed. This allows time for a naive T cell to interact with antigen-presenting cells and be activated. Activated T cells also transiently express the protein CD69, which binds to and down regulates S1PR1, thus enabling the T cell to remain in the lymph node long enough to complete the initial activation program. Following activation, the T cell loses CD69 and, since it is not exposed to S1P, it re-expresses S1PR1 and is thus directed down the S1P concentration gradient out of the lymph node and into the efferent lymphatics. Fingolimod interferes with this process, so that T cells remain trapped within lymph node and thymus.

69
Q 
Which of the following is a proinflammatory cytokine of major importance in innate immunity that has been successfully targeted by drugs to treat rheumatoid arthritis (RA)?
Tumor necrosis factor (TNF)
Transforming growth factor-β (TGF-β)
Interleukin 10
Interleukin 2
Interferon γ
A

TNF is secreted by macrophages in response to PAMPs and DAMPs and mediates acute inflammatory responses by activating endothelial cells and leukocytes. Anti-TNF antibodies and recombinant soluble TNF receptor-IgG fusion proteins have been highly successful in treating RA.

70
Q

Toll like receptors (TLRs) located in endosomal membranes of cells recognize which of the following?
Nucleic acids
Bacterial cell wall lipotechoic acid
Bacterial cell wall lipopolysaccharide
Uric acid crystals
Peptides containing N-formylmethionyl residues

A

Endosomal TLR-3,-7, and -9, recognize dsRNA, ssRNA, and CpG dinucleotides which are components of ingested viruses (dsRNA, ssRNA) and other microbes (unmethylated CpG-rich oligonucleotides). Bacterial cell wall lipotechoic acid and lipopolysaccharide are recognized by plasma membrane TLRs. Uric acid crystals are recognized by cytosolic NLR proteins in inflammasomes, and bacterially derived peptides containing N-formylmethionyl residues are recognized by the plasma membrane fmet-leu-phe receptor.

71
Q

Microbial DNA stimulates innate immune responses through which of the following pathways?

  • Plasma membrane TLR9 leading to activation of NF-κB
  • Cytosolic RIG-like receptors leading to activation of interferon regulatory factors (IRFs)
  • Blood C-reactive protein (CRP) leading to complement activation
  • Cytosolic cyclic dinucleotides and endospermic STING leading to activation of interferon regulatory factors (IRFs)
  • Plasma membrane mannose-binding lectin (MB) leading to complement activation
A

Microbial ds DNA in the cytosol induces synthesis of cyclic dinucleotides, which bind to endoplasmic STING, leading to signaling events that activate IRFs, which induce type I interferon production. TLR9 does respond to DNA in endosomes, not the cytosol. Neither CRP or MBL recognize or respond to DNA.

72
Q 
All of the following molecules are opsonins that facilitate efficient phagocytosis of microbes by neutrophils and macrophages EXCEPT:
C3b
C5a
C-reactive protein
IgG
Mannose-binding lectin
A

C5a is a peptide released after cleavage of C5 protein upon activation of the complement cascade. It stimulates the influx of neutrophils to the site of infection, thus acting as a chemoattractant, not as an opsonin. C3b (covalently bound to microbes on which complement activation has taken place) and IgG bound to antigen, are potent opsonins, because phagocytes have receptors for both C3b and the Fc region of IgG. C-reactive protein and mannose-binding lectin also can coat microbes and be recognized by phagocyte receptors; thus they serve as opsonins.

73
Q

Which of the following is a feature of Natural Killer (NK) cells?

  • They express clonally distributed antigen receptors that directly bind antigens on the surface of microbes
  • They are activated by recognizing microbial peptides bound to host class I MHC molecules
  • They kill virally infected cells by a perforin/granzyme dependent mechanism
  • Upon activation, they secrete abundant interleukin-4
  • They secrete natural IgM antibodies
A

Upon activation, NK cells release perforin and granzymes from cytoplasmic granules, and these proteins work together to induce apoptosis of the target cell. NK cells are activated by binding various ligands expressed on infected or stressed target cells. NK cells are inhibited by binding self class I MHC, a feature of healthy cells, but often not of virally infected or otherwise unhealthy cells. NK cells secrete several cytokines, including IFN-γ, but they do not secrete IL-4.

74
Q 
Detection of antibodies specific for a particular microbe is commonly used as evidence of prior infection by that microbe. To obtain these antibodies, blood is collected into tubes and allowed to clot. Antibodies are found in the fraction of the blood that remains fluid after clotting. What is this fluid fraction called?
Plasma
Serum
Lymph
Water
Urine
A

Clots form from the cellular elements of blood, including platelets, and a meshwork of cross-linked coagulation proteins. The acellular fluid phase that is left after clotting is called serum, which contains most of the soluble protein elements of whole blood, except clotting factors. Plasma is the acellular fluid fraction of unclotted blood, and apart from coagulation proteins that form the clot, it contains all of the soluble protein components of whole blood, including antibodies. Lymph is extracellular fluid derived from blood; it may contain antibodies. Urine is the fluid filtrate of blood exclusively produced and excreted by the kidneys. It normally does not contain antibodies.

75
Q

Which one of the following is a correct description of the basic symmetric core structure of an IgG antibody?
One heavy chain and two light chains
One constant domain and one variable domain.
Two heavy chains and one light chain
Two heavy chains and two light chains
One heavy chain and one light chain

A

Two γ heavy chains are covalently linked to each other, and each heavy chain is covalently linked to one light chain (κ or λ). IgM molecules contain 5 covalently linked copies of the basic IgM core structure, and IgA contain two copies. Each IgG heavy chain has one variable domain and three constant domains, and each light chain has one variable domain and one constant domain.

76
Q

An antigen-binding site of an IgG antibody molecule is composed of which of the following?
Twelve hypervariable loops, three each on two heavy chains and two light chains
Three hypervariable loops on a light chain
Three hypervariable loops on a heavy chain
Six hypervariable loops, three each on one heavy chain and one light chain
Six hypervariable loops, three each on two heavy chains

A

An IgG molecule has two antigen binding sites. Each one is composed of six hypervariable loops, three that extend from the variable domains of a heavy chain and three that extend from the variable domains of the covalently linked light chain.

77
Q

IgG has a longer half life in the blood than most other plasma proteins. This property is important for maintaining protection against pathogens, and has lead to the design of drugs with long half lives because they contain the part of IgG responsible for the long half life. Which of the following is the basis for prolonged IgG half life?

  • Binding of C1q to the IgG Fc region
  • Binding of the IgG Fc region the poly Ig receptor on gut epithelial cells
  • Binding of the IgG variable regions to ubiquitous blood antigens
  • Binding of the J chain to the IgG joining region
  • Binding of the IgG Fc region to the neonatal Fc receptor (FcRn)
A

IgG molecules are internalized by endothelial cells and macrophages, and bind the FcRn in the membrane of endosomes. FcRn sequesters the IgG molecules, shunting them away from lysosomal degradation, and releases them back into the circulation.

78
Q 
Which of the following is the most important antigen presenting cell for activation of naive CD4+ T cells in lymph nodes?
B cells
Macrophages
Mast cells
Neutrophils
Dendritic cells
A

Dendritic cells take up protein in tissues, carry them through the lymph into lymph nodes, and present peptides derived from the proteins to naïve T cells that recirculate through the nodes. Dendritic cells express costimulatory molecules and class II MHC molecules. These properties make dendritic cells the only cell type that can efficiently present and activate naive CD4+ T cells. B cells and macrophages can present antigen to CD4+ T cells, but they mainly activate helper T cells, not naïve T cells. Mast cells and neutrophils have little or no antigen presenting capabilities.

79
Q

Which of the following accurately describes HLA gene expression by a single dendritic cell in an individual.
Only class II HLA genes
Only class I MHC genes
Only one of the two inherited HLA alleles for each Class I and class II HLA gene
All inherited class I and class II HLA alleles
No HLA genes

A

HLA (MHC) genes are codominantly expressed, meaning both maternal and paternal inherited alleles of each HLA gene are expressed simultaneously in cells that can express HLA genes. Dendritic cells express both class I and class II HLA, and therefore they simultaneously express both inherited alleles of the class I genes ( HLA-A, -B, and -C) and both inherited alleles of the class II genes ( HAL-DP, -DQ, and- DR).

80
Q 
Which of the following is the nonpolymorphic molecule that is structurally homologous to the class I MHC α chain, associates with β2-microglobulin, and displays lipid antigens for recognition by NKT cells?
CD1
CD2
CD3
CD4
CD8
A

CD1 is encoded outside the MHC, but is structurally homologous to class I MHC molecules. Some subsets of T cells, all with relatively invariant T cell receptors, recognize lipid or glycolipid antigens bound to CD1 on antigen-presenting cells. CD2, CD3, CD4, and CD8 are all present on T cells. Although they are members of the Ig superfamily, like class I MHC, they are not otherwise homologous to class I MHC and do not bind and display antigens for T cell recognition.

81
Q

Which one of the following statements about peptide binding to MHC molecules is true?

  • MHC molecules preferentially bind peptides derived from foreign (e.g., microbial) proteins and not peptides derived from self proteins.
  • Each type of MHC molecule and each allelic variant of each type have a narrow specificity for a single peptide with a particular amino acid sequence.
  • The affinity of peptide binding to MHC molecules is higher, on average, after chemokine stimulation of a cell.
  • An MHC molecule has only one peptide-binding site, which accommodates only a single peptide at a time.
  • Peptide binding to class I MHC molecules involves noncovalent interactions, whereas peptide binding to class II MHC molecules is covalent.
A

There is only one peptide-binding site in both class I and class II MHC molecules that can fit only a single peptide at one time. MHC molecules do not distinguish foreign from self proteins; self-nonself discrimination is achieved by T cells. Each MHC molecule has a broad specificity for large numbers of peptides with varying sequences, although there are some structural constraints that result in each type of MHC molecule binding a different subset of peptides. The affinity of peptide-MHC interactions is not altered by chemokines. Peptide binding to both class I and class II MHC molecules involves only noncovalent interactions.

82
Q 
In the class I MHC pathway of antigen presentation, peptides generated in the cytosol are translocated into the endoplasmic reticulum in which of the following ways?
By ATP-dependent transport via TAP
By passive diffusion
By receptor-mediated endocytosis
Through membrane pores
Via the proteasome
A

The TAP1/TAP2 heterodimer is an ATP-dependent pump that delivers peptides generated by the proteasome into the endoplasmic reticulum. The proteasome is a proteolytic organelle in the cytosol that generates the MHC-bind peptides from proteins, prior to TAP transport of the peptides into the endoplasmic reticulum.

83
Q 
In the class I MHC pathway of antigen presentation, cytoplasmic proteins are tagged for proteolytic processing by covalent linkage with which of the following molecules?
Calreticulin
Nuclear factor (NF)-κB
Tapasin
Ubiquitin
Calnexin
A

In the class I pathway, proteins are tagged for proteasomal processing by covalent addition of several copies of the polypeptide ubiquitin. Ubiquitin-dependent proteasomal proteolysis is also important in many other cellular processes besides antigen presentation. For example, NF-κB is a transcription factor whose activation is dependent on ubiquitination and proteasomal degradation of an inhibitor (called IκB). Calreticulin, tapasin, and calnexin regulate the assembly of class I MHC proteins within the endoplasmic reticulum.

84
Q

MHC genes are the most polymorphic of any in the human genome. Which of the following statements about MHC polymorphism is true?

  • HLA-A, HLA-B, and HLA-C represent three different alleles of the same gene.
  • Most of the polymorphic residues in any MHC protein are located in the peptide binding groove.
  • Only class I MHC genes are polymorphic; class II MHC genes are not.
  • Many unrelated people have identical MHC alleles
  • MHC polymorphism is a result of somatic recombination of inherited nonpolymorphic MHC gene segments.
A

MHC polymorphism are concentrated in the peptide binding groove, resulting in differences in the range of peptides that can bind to each allelic form on each type of class I or class II MHC molecules. HLA-A,-B, and –C are different types of class I MHC molecules, encoded by three different genes, each one of which has many different alleles in the population. It is very rare for two individuals to have identical sets of HLA alleles, unless they are siblings. Both class I and class II MHC genes are polymorphic, although class I MHC genes are more polymorphic. MHC genes are not somatically rearranged, but rather the allelic variations are encoded in the germline and are inherited.

85
Q 
Which of the following is an example of G protein-coupled receptor (GPCR)?
T cell antigen receptor (TCR)
The B cell antigen receptor (BCR)
CD4
Interlukin-2 (IL-2) receptor
Chemokine receptor CCR7
A

All chemokine receptors, including CCR7, are GPCRs. The lymphocyte antigen receptors (TCR, BCR), CD4, and IL-2 receptor signal via associated proteins or non-receptor tyrosine kinases.

86
Q

The cytoplasmic tails of the signaling polypeptides found in lymphocyte antigen receptor complexes (BCR and TCR) contain regions that become phosphorylated upon antigen recognition and then bind ZAP family kinases. These regions are called:
Immunoreceptor tyrosine-based activating motifs (ITAMs)
Fc regions
Toll-like IL-1R (TIR) domains
Complementarity determining regions
Nod like receptor ( NLR) domains

A

ITAMs are found in the cytoplasmic tails of CD3 and ζ proteins of the TCR complex and Igα and Iβ proteins of the BCR complex. ITAMs contain pairs of tyrosine residues that become phosphorylated by Src family kinases after antigen recognition, and then serve as docking sites for ZAP70 in T cells or Syk in B cells. ZAP70 and Syk are tyrosine kinases that become active after binding to ITAMs and then phosphorylate adaptor proteins and other kinases.

87
Q

What role does CD4 and CD8 on T cells play in the early signaling events during T cell activation?

  • Like CD3 and ζ proteins, CD4 and CD8 contain ITAMs in their cytoplasmic tails that serve as docking sites for protein tyrosine kinases (PTKs)
  • CD4 and CD8 have intrinsic phosphatase activity in their cytoplasmic tails that remove phosphates from ITAMs on CD3 and ζ proteins
  • When CD4 and CD8 bind to MHC molecules on antigen presenting cells, the MHC molecules become active kinases that activate the APCs
  • CD4 and CD8 have Src family PTKs associated with their cytoplasm tails, which are brought into proximity of and phosphorylate the CD3 and ζ ITAMs upon antigen recognition.
  • Upon antigen recognition, the cytoplasmic tails of CD4 and CD8 became phosphorylated and bind JAK family kinases, which then phosphorylate STAT family proteins.
A

Lck, a Src family PTK, is noncovalently associated with the cytoplasmic tails of both CD4 and CD8, and Lck phosphorylates CD3 and ζ chain ITAMs when CD4 and CD8 bind to MHC molecules during antigen recognition. CD4 and CD8 do not have ITAMs, intrinsic kinases, phosphatases or JAK kinase binding sites in their cytoplasmic tails. MHC molecules also do not have intrinsic kinase activities.

88
Q 
In the T cell calcium signaling pathway induced by antigen recognition, which enzyme and transcription factor are activated?
IκB kinase, NFκB
Jun kiniase (JNK), AP-1
Erk kinase, Fos
JAK3, STAT4
Calcineurin, NFAT
A

In the calcium pathway, TCR signaling leads to an increase in cytosolic calcium ion (Ca++) concentration, which activates the phosphatase calcineurin, leading to dephosphorylation of the transcription factor NFAT. Dephosphorylated NFAT enters the nucleus and stimulates transcription of various genes that promote T cell proliferation and differentiation. Calcineurin inhibitors, such as cyclosporin and tacrolimus, are widely used as immunosuppressant drugs for transplant recipients

89
Q

How does the complement system enhance B lymphocyte activation?

  • Generation of the membrane attack complex on B cell membrane allows calcium ions (Ca++) to enter the B cell and stimulate calcium-dependent enzymes
  • Opsonization of protein antigens with C3b promotes B cell phagocytosis of protein antigens, enhancing B cell-T cell collaboration
  • C1q binding to membrane IgM will activate BCR signaling
  • C3d bound to a microbial surface will bind to complement receptor 2 (CR2) on B cells, generating kinase activity by the CR2-CD19-CD81 complex
  • C5a binding to its receptor on B cells stimulates Ig heavy chain gene expression
A

CR2 is expressed on B cell membranes in a complex with CD19 and CD81. CR2 binds to C3d, a proteolytic product of C3b that remains covalently bound to microbial surfaces after complement activation. If CR2 binds C3d on a microbe at the same time that microbial surface antigens bind to membrane Ig, signaling through the CR2-CD19-CD81 complex enhances BCR signaling resulting in enhanced B cell activation.

90
Q

Which of the following proteins involved in attenuation of immune signaling become associated with immunoreceptor tyrosine inhibitory motifs (ITIMs)?
E3 ubiquitin ligases
SH2 domain-containing tytrosine phosphatases (SHP-1, SHP-2)
Suppressors of cytokine signaling (SOCS)
CTLA-4
PD-1

A

ITIMs are found in the cytoplasmic tails of inhibitory receptors on NK cells, T cells, and B cells. ITIMs bind SHP-1, SHP-2, and SH2 domain-containing inositol phosphatase (SHIP). SHP-1, SHP-2 remove phosphates from tyrosines in signaling intermediates downstream of activating receptors. SHIP removes phosphates from phospholipid signaling intermediates also downstream of activating receptors. The other choices are not associated with ITIMs. E3 ubiquitin ligases are intracellular enzymes that tag proteins for lysosomal and proteosomal degradation, and some E3 ubiquitin ligases, such as Cbl-b, are involved in endocytosis and degradation of the TCR. Suppressors of cytokine signaling (SOCS) inhibit JAK-STAT and TLR signaling. CTLA-4 and PD-1 are membrane proteins that inhibit T cell activation when they bind ligands on other cells.

91
Q 
A one year old boy with a history of severe infections is found to have very few circulating mature T cells or NK cells, but normal numbers of B cells. Genetic studies reveal he has X-linked severe combined immunodeficiency syndrome. Defective signaling by the receptor for which cytokine is the underlying cause of this disease?
IL-1
IL-2
IL-4
IL-7
GM-CSF
A

X-linked severe combined immunodeficiency syndrome (X-linked SCID) caused by mutations in the common γ chain which is a signaling polypeptide in the multimeric cytokine receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. Although signaling from all of these receptors would be defective in X-linked SCID, only IL-7 is required for early development of T cells and NK cells in the thymus of humans.

92
Q

In both B and T cell development, there is stage when a pre-antigen receptor (pre B cell receptor or pre T cell receptor) is expressed. Which of the following accurately describes an important function of these pre-antigen receptors?

  • Positively select for lymphocytes that have successfully undergone a first round of V-D-J recombination required to express functional antigen receptors
  • Negatively select for self-reactive lymphocytes
  • Instruct the differentiation of the lymphocytes into different subsets of effector cells
  • Positively select lymphocytes that recognize microbial antigens
  • Bind to chemokines that keep the lymphocytes from migrating out of the generative lymphoid organs
A

Signals generated by the pre-antigen receptors are required for survival of developing lymphocytes. Since the pre B cell receptor contains an Ig μ heavy chain, and the pre T cell receptor contains a TCR β chain, only developing lymphocytes that have successfully rearranged Ig μ or TCR β genes will survive, and have a chance of rearranging and expressing Ig light chain or TCR α chain genes. Therefore, the pre-antigen receptors provide a checkpoint mechanism by which useless cells that will never be able to express an antigen receptor are purged. The pre-antigen receptors do not stimulate lymphocyte differentiation into effector cells, but they do stimulate proliferation and further molecular events in development of mature naïve lymphocytes. Since pre-antigen receptors are not fully formed antigen receptors, they cannot mediate selection for or against self or foreign antigens, and they have no chemokine binding capacity.

93
Q

Which of the following mechanisms contributes most to both Ig and TCR diversity?

  • Multiple possible combinations of the different V, D, and J segments
  • Changes in the nucleotide sequences at the junctions between recombined V, D, and J segments
  • Somatic mutation of variable genes
  • Isotype switching
  • Polymorphism
A

Junctional diversity is caused by deletions and additions of base pairs between V, D, and J segments during somatic recombination, resulting in new junctional sequences not present in in inherited (germline) DNA. This accounts for the majority of Ig and TCR diversity. Combinatorial diversity is the second major mechanism for diversity, based on the large number of different V, D, and J segments inserted in the germline that can be used during somatic recombination, but it contributes much less to diversity than does junctional variability. Somatic mutation of variable genes occurs during the germinal center reaction in B cells only, and its impact on diversity is far less than the mechanism of junctional diversity. Isotype switching (of Ig molecules only) changes the non–antigen-binding region and does not contribute to diversity of antigen receptor specificity. Polymorphism refers to the presence of different alleles of a gene in the population, not in an individual, and is not a mechanism of diversity of the antigen receptor repertoires.

94
Q

Which enzyme contributes to antigen receptor junctional diversity by adding random nucleotides at the junctions between V, D, and J segments and is also useful as a marker of neoplasia of pro-B and pro-T cells?
Terminal deoxyribonucleotidyl transferase (TdT)
Activation-induced deaminase (AID)
Recombinase activating gene-1 (RAG-1)
DNA-dependent protein kinase
DNA polymerase

A

Terminal deoxyribonucleotidyl transferase (TdT) is the enzyme that adds random nontemplate nucleotides (called N nucleotides) at the junctions between V, D and J segments, mainly in the recombined Ig heavy chain and TCRβ chain genes. The enzyme is expressed mainly during the time in B cell and T cell development when the IgH and TCR β chain genes are undergoing recombination. Activation-induced deaminase is an enzyme involved in somatic mutation and isotype switching of Ig genes. Recombinase activating gene-1 (RAG-1) is a component of the V(D)J recombinase that mediates the joining of the discrete gene segments, and DNA-dependent protein kinase participates in the recombination and joining process, but these enzymes do not contribute on their own to junctional diversity.

95
Q

Why do Ig and TCR genes only undergo rearrangements in B and T cells and not other cell types?
The hepatmer/nonamer recombination signal sequences (RSSs) adjacent to V, D, and J gene segment are present only in B and T cells
The Ig and TCR α genes are deleted in other cell types
Recombinase activating genes (RAG-1 and RAG 2) are expressed only in developing lymphocytes
Activation induced deaminase (AID) is expressed only in developing lymphocytes
DNA-dependent protein kinase is only expressed in developing lymphocytes

A

A complex of RAG-1 and RAG-2 is the V-(D)-J recombinase that recognizes RSSs adjacent to V, D, and J gene segment, and cuts the DNA at these locations. This is an essential step for V-(D)-J rearrangements. The RAG proteins are only expressed in developing B and T cells, and only at certain times during development. The actual inherited Ig and TCR gene sequences in developing lymphocytes before recombination occurs, including coding gene segments and RSSs, are identical to the sequences in all other cells. AID is required for Ig gene switch recombination and somatic mutation of Ig V genes, but does not play a role in antigen receptor V-(D)-J rearrangements. DNA-dependent protein kinase is a DNA repair enzyme necessary but not sufficient for the antigen receptor rearrangements, and it is not unique to B and T cells.

96
Q 
Which of the following mechanisms accounts for the fact that all of the TCRs produced by a single T cell have identical β chains?
X inactivation
Light chain isotype exclusion
Antigen receptor gene homozygosity
Linkage disequilibrium
Allelic exclusion
A

In TCR allelic exclusion, expression of the β chain gene encoded by a successfully recombined gene on one chromosome inhibits recombination of the β chain gene on the other chromosome. The inhibitory signals are generated by the pre-TCR. This ensures that the T cell will not produce receptors with two different β chains. However, allelic exclusion does not occur for TCR α chain genes, and many T cells may express TCRs with two different α chains. Heavy chain allelic exclusion occurs by a similar mechanism in B cell development.

97
Q

Receptor editing is a mechanism to achieve self tolerance if a self reactive lymphocyte develops. How, where, and when does self editing work?
High avidity self antigen recognition by an immature B cell in the bone marrow leads to reactivation of RAG genes, production of a new Ig light chain, and a change in the B cell specificity.
High avidity self antigen recognition by an immature T cell in the thymus leads to production of a new TCR and a change in the T cell specificity.
High avidity self antigen recognition by an immature B cell in the bone marrow leads to enzymatic alteration of Ig light chain proteins, and a change in the B cell specificity.
High avidity self antigen recognition by an immature T cell in the thymus leads to enzymatic alteration of the TCR α chain, and a change in the T cell specificity.
High avidity self antigen recognition by an immature B cell in the bone marrow leads to reactivation of RAG genes, additional heavy chain V-D-J recombination events, production of a new Ig heavy chain, and a change in the B cell specificity.

A

Receptor editing occurs only in immature B cells in the marrow after high avidity recognition of self antigens, is due to re-expression of the RAG-1 and -2 genes and rearrangement of a previously rearranged Ig light chain gene locus.

98
Q

Innate immune responses can involve:

a. B lymphocytes
b. T lymphocytes
c. Natural Killer Cells
d. Antibodies

A

NK cells

99
Q 
Adaptive immune responses typically start to develop approximately \_\_ after exposure to
infectious microbe:
a. Immediately
b. 6 hours
c. 1 day
d. 4 days
A

1 day

100
Q

Innate immune response is characterized by:

a. Immune responses specific for distinct antigens
b. Recognition of molecules shared by groups of related microbes
c. Ability to recognize very large number of antigens (diversity)
d. Immunologic memory- secondary response is stronger than primary response

A

Recognition of molecules shared by groups of related microbes

101
Q

An advantage of passive immunization compared to active immunity is that it provides:

a. Rapid resistance to infection
b. Specific response to microbial antigens
c. Immunologic memory
d. Transfer of lymphocytes from mother to fetus

A

Rapid resistance to infection

102
Q

These types of lymphocytes recognize antigens on the surfaces of antigen-presenting cells and
secrete cytokines, which activate macrophages, produce inflammation and activate other T and B
lymphocytes:
a. Regulatory T lymphocyte
b. Helper T lymphocyte
c. B lymphocyte
d. Cytotoxic T Lymphocyte

A

Helper T lymphocyte

103
Q

This type of immune cell is involved in antibody-mediated neutralization of microbes, where
antibodies bind to microbes and prevent them from infecting cells:
a. Regulatory T lymphocyte
b. Helper T lymphocyte
c. B lymphocyte
d. Cytotoxic T Lymphocyte

A

B lymphocyte

104
Q 
This type of immune cell is the most efficient at killing intracellular microbes and eliminating
reservoirs of infection:
a. Regulatory T lymphocyte
b. Helper T lymphocyte r
c. B lymphocyte
d. Cytotoxic T Lymphocyte
A

Cytotoxic T Lymphocyte

105
Q

A cardinal feature of the adaptive immune response is self tolerance (non reactivity to self),
which mediated by these types of cells which function mainly to inhibit immune responses:
a. Memory B cells
b. Regulatory T lymphocyte
c. Plasma cells
d. Helper T cells

A

Regulatory T lymphocyte

106
Q

The adaptive immune response is initiated when naive T and B lymphocytes recognize antigen. The next step in the adaptive immune response after recognition is:

a. Production of memory B and T cells C
b. Differentiation of lymphocytes into antibody-producing cells and effector T lymphocytes
c. Clonal expansion of lymphocytes (proliferation into antigen-specific clones)
d. Elimination of antigen by antibodies and effector T cells

A

The adaptive immune response is initiated when na”ive T and B lymphocytes recognize antigen.
The next step in the adaptive immune response after recognition is:
a. Production of memory B and T cells C
b. Differentiation of lymphocytes into antibody-producing cells and effector T lymphocytes
c. Clonal expansion of lymphocytes (proliferation into antigen-specific clones)
d. Elimination of antigen by antibodies and effector T cells

107
Q

These are a large group of secreted proteins which regulate and coordinate many activities of
the cells of both innate and adaptive immunity:
a. Antibodies
b. Complement D
c. MHC molecules
d. Cytokines

A

Cytokines

108
Q

The most abundant white blood cell present in the bloodstream is ___

a. Lymphocytes
b. Monocytes
c. Eosinophils
d. Neutrophils
e. Monocytes

A

Neutrophils

109
Q 
How many neutrophils are produced in an adult in any given day?
a. 1 X 10 11
b. 1x105
C. 1 X 10 3
d. 100
e. 10
A

1 X 10 11

110
Q 
Classical monocytes are recognized by which of the following CD markers?
a. CO2
b. CD16
C. CD14
d. CD4
e. CDS
A

CD14

111
Q

Which of the following cytokines is crucial in mast cell development?

a. IFN-y
b. IL-2
c. Stem cell factor
d. IL-5

A

Stem cell factor

112
Q

Dendritic cells are professional antigen presenting cells that can display antigens to
lymphocytes using which of the following?
a. MHC Class I molecules
b. MHC Class II molecules
c. Both A and B
d. · None of the above

A

Both MHC Class I molecules AND MHC Class II molecules

113
Q

Which of the following cytokines is crucial in maintaining survival of naive T cells?

a. IL-4
b. IL-5
c. IL-6
d. IL-7
e. IL-8

A

IL-7

114
Q

CD4+ Th1 cells depend on which transcription factor?

a. GATA-3
b. RORyT
c. T-bet
d. STAT 6
e. STAT 5

A

Th1 – T-bet, STAT1, STAT4
Th2 – GATA-3, STAT6
Th17 – RORyT
Treg – STAT5

115
Q

The organization of cells within the lymph node is achieved using chemokines.
Chemokines important in directing Naive T cells to appropriate locations would be
a. CCL 19 and CCL20
b. CCL20 and CCL21
c. CCL22 and CCL25
d. CCL 19 and CCL21

A

CCL 19 and CCL21 (CCR7 is the receptor)

116
Q

Knockout mice lacking CXCR5 will not have which of the following in lymph nodes?

a. NK Cells
b. T Cells
c. B Cells
d. Follicular Dendritic Cells

A

B cells (CXCL13 is the chemokine); no follicles

A/I Board Review (1 decks)

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