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Clinical Immunology > Cellular Activities and Clinical Disorders > Flashcards

Cellular Activities and Clinical Disorders Flashcards

1
Q

What are the steps of phagocytosis?

A
  1. Chemotaxis
  2. Adhesion
  3. Engulfment
  4. Digestion
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2
Q

What happens during chemotaxis in phagocytic signaling?

A

Neutrophils arrive within 1 hour due to attraction to chemicals, such as antigens (chemoattractants). Monocytes, macrophages, and DCs arrive later. Speed of phagocytosis sped up due to Fc receptor and C3 opsonization

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3
Q

What happens during adhesion in phagocytosis?

A
  1. Tethering (particle contact)
  2. Triggering (PMN prepped to get cytokine signal)
  3. Adhesion (integrins promote CAMs on endothelium, so inflammatory response begins due to release of inflammatory chemicals)
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4
Q

What happens during engulfment in phagocytosis?

A

Bacteria engulfed through active membrane invagination. Pseudopodia are pulled by interactions between Fc receptors and Fc antibody portions on the opsonized bacterium until the pseudopodia meet and fuse

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5
Q

What happens during digestion in phagocytosis?

A

Granules (aka lysosomes) in the phagocyte migrate and fuse with the phagosome to form the phagolysosome

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6
Q

What are the 3 types of degradatory enzymes? What are examples of each?

A
  1. Primary/azurophilic granules: enzymes such as lysozyme and myeloperoxidase)
  2. Secondary/specific granules: lactoferrin
  3. Tertiary granules: caspases (cleave proteins for apoptotic signaling)
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7
Q

Which neutrophil bacterial killing mechanism is more important? Oxidative or non-oxidative?

A

Oxidative/oxygen-dependent

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8
Q

What can happen if bacteria are not phagocytosed?

A

They may establish at secondary sites like the lymph nodes. Bacteremia may develop

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9
Q

What are Neutrophil Extracellular Traps (NETs)?

A

These are innate immune components composed of antimicrobial proteins and chromatin + histones

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10
Q

What are 3 monocyte-macrophage defense functions?

A
  1. Phagocytosis
  2. APC
  3. Secrete cytokines (aka “biologically active molecules”)
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11
Q

Give examples of chemoattractants for monocytes

A

Complement products
Chemokines from neutrophils, lymphs, or cancer cells

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12
Q

True of False: Macrophages kill only extracellular pathogens

A

FALSE. Can kill intracellular pathogens, such as parasites, Mtb, and some fungi

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13
Q

Which cytokine do monocytes-macrophages primarily release? What is it’s function?

A

IL-1
Inflammatory response

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14
Q

Give examples of biologically active molecules that monocytes-macrophages synthesize

A

Transferrin
Complement
IFN
Pyrogens
Growth factors

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15
Q

Describe Macrophage Activation Syndrome

A

It’s a cytokine storm syndrome (CSS) that involves dysregulated macrophages, which leads to excessive cytotoxic T cells and macrophage proliferation. This leads to excessive proinflammatory cytokine production, thus creating a cytokine storm

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16
Q

Define inflammation

A

Immune response resulting in complete elimination of pathogen, followed by resolution of tissue damage, full regeneration of tissue function, and disappearance of leukocytes from the tissue

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17
Q

Describe the different immune cell populations in acute and chronic inlammation

A

Acute: More neutrophils and activated T lymphs than chronic

Chronic: macrophages, Tc cells, B cells

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18
Q

List the 3 major stages of inflammation

A
  1. Capillary dilation to increase blood flow
  2. Microvascular structural changes the escape of plasma proteins from the bloodstream
  3. Leukocyte transmigration through endothelium and accumulation at the site of the injury
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19
Q

Define sepsis. What causes it?

A

It is systemic inflammatory response syndrome (SIRS) + infection. Caused by innate immune system aggressively responding to bacterial presence

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20
Q

Define severe sepsis

A

Sepsis + evidence organ dysfunction

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21
Q

Which PRR cause APCs to produce proinflammatory cytokines?

A

TLRs

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22
Q

Which biochemical markers are associated with sepsis?

A

IL-1, IL-6, and TNF
Procalcitonin
Chemokines
C-reactive protein (CRP)

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23
Q

List 3 cell surface receptor families

A
  1. Ig
  2. Integrins
  3. Selectins
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24
Q

What happens during Non-infectious Neutrophil-Mediated Inflammatory Disease?

A

Neutrophils become destructive to host tissue through oxidative and non-oxidative mechanisms. Inappropriate phagocytosis. Caused by prolonged oxidative response, so ROS damage to host

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25
Q

What happens during Abnormal Neutrophil Function?

A

Neutropenia or severe functional defects.
tissue. Leukocyte mobility may be impaired. Suffer from recurrent bacterial (esp. pneumonia) infections, fungal infections

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26
Q

What happens during Chronic Granulomatous Disease (CGD)?

A

X-linked disease where neutrophils only kill streptococci but NOT staphylococci. Can still phagocytose, but not kill, non-peroxide producing bacteria. Suffer from catalase-positive bacterial infections, fungal infections, and granulomas. Failure to exhibit increased anaerobic metabolism during phagocytosis

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27
Q

What happens during Chediak-Higashi Syndrome?

A

Abnormal granulation (they’re giant granules) such that neutrophils suffer from impaired chemotaxis and delayed killing of phagocytosed bacteria

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28
Q

What happens during CR3 Deficiency?

A

Marked abnormalities in adherence functions, leads to Leukocyte Adhesion Disorders (LAD) and reduced inflammatory response, neutrophilia, poor phagocytosis of opsonized pathogen, and reduced diapedesis/chemotaxis

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29
Q

What happens during Myeloperoxidase Deficiency. What is myeloperoxidase?

A

Defective bacterial/fungal killing. Generally healthy patients but diabetics suffer from Candida spp. infections. Myeloperoxidase is an iron-containing heme protein responsible for peroxidase activity of azurophilic granules

30
Q

What happens in Specific Granule Deficiency?

A

Failure to synthesize granules during blood cell differentiation in the BM. Leads to recurrent, severe bacterial infections of the skin and deep tissues and depressed inflammatory response

31
Q

What are two monocyte-macrophage (M-M) disorders? What do the two diseases have in common?

A
  1. Gaucher disease
  2. Niemann-Pick disease (Types A, B, and C)

Both involved impaired lipid metabolism

32
Q

What happens in Gaucher disease?

A

Impaired lipid metabolism leads to impaired phagocytosis, monocyte cytotoxicity, and macrophage-activating factors. Cell debris build up that macrophages usually clear

33
Q

What happens in Niemann Pick Disease?

A

Types A + B: Sphingomyelinase defect prevents the conversion of sphingomyelin to ceramide, leading to sphingomyelin buildup inside monocytes

Type C: Can’t break down cholesterol so get cholesterol buildup in liver, spleen, and other lipids in brain

34
Q

Describe Leukocyte Adhesion Deficiency (LAD)

A

Leukocytes can’t adhere to endothelial lining. Leads to recurrent and often fatal bacterial and fungal infections. Two genotypes: LAD-1 and LAD-2

35
Q

What are cell surface markers used for?

A
  1. ID lymph subsets
  2. Establish lymph maturity
  3. Classify leukemias and lymphomas
  4. Monitor patients on immunosuppressive therapy
36
Q

What are the CD markers for Tc and Th cells?

A

Tc = CD3 and CD8
Th = CD3 and CD4

37
Q

What is the CD marker for NK cells?

A

CD16

38
Q

What are the CD markers for B cells? Plasma cells?

A

CD19 and CD21. Plasma cells lose the CD19 marker

39
Q

Describe double-negative thymocytes

A

They’re early thymocytes that lack both CD4 and CD8, but still express CD3. IL-7 stimulates their proliferation and differentiation in the outer cortex of thymus. Increased in lymphoproliferative disorders, graft vs host disease, and autoimmune diseases

40
Q

Describe double-positive thymocytes (Which CDs are expressed, selection process, act like what kind of cell, presence in which diseases)

A

Cells that express both CD4 and CD8, in addition to CD3. In positive selection, these T cells recognize both MHCI and MHCII. May act like NK cells. Present in inflammatory diseases, viral infections, and cancer.

41
Q

Describe T lymph maturation/differentiation after they leave the thymus

A

Migrate to medulla, then exit into peripheral blood where they gain functional maturity

42
Q

Describe the properties of Th1 cells

A

-Defense against intracellular pathogens
-Resistance to mycobacterial infections
-Autoimmune disease induction
-IFN-gamma stimulates differentiation of Th cells into Th1

43
Q

Describe properties of Th2 cells

A

-Play greater role in mediating antibody production
-Mediates defense against extracellular parasites (e.g., helminths)
-Induces asthma/allergic inflammatory diseases
-IL-4 stimulates Th differentiation into Th2

44
Q

Describe properties of Th17 cells

A

-Play important role in protection against bacteria and fungi (extracellular pathogens)
-Induces many organ-specific diseases
-IL-21 amplifies differentiation into Th17 cells

45
Q

Describe properties of CD8+ T lymphs

A

-In peripheral blood
-Directly destroy virally infected target cells
-In primary viral infection: naive Tc cells primed in secondary lymph nodes, then proliferate and differentiate into effector cells to kill virus
-Major effectors in allograft organ rejection
-SUPPRESSOR T LYMPHS (Ts) tend to be CD8+!!! Downregulate actions of other T and Be cells

46
Q

Which types of antigens to each Th and Tc cells recognize?

A

Helper T cells recognize phagolysosomal antigens (meaning that they were extracellular and got phagocytosed)

Cytotoxic T cells recognize cytoplasmic antigens (meaning that they were intracellular like in viral protein production)

47
Q

How many antigen receptors does each lymph makes?

A

ONE

48
Q

What does T cell activation lead to?

A

-Cell division
-Cytokine secretion by T cells
-Expressing antigens associated with activated state

49
Q

Describe CD4+ T cell responses to viral infection

A

-Activate B cells for Ab synthesis
-Induce macrophages to enhance killer activity
-Recruit granulocytes to sites of infection/inflammation, and make chemokines

50
Q

Describe Cd8+ T cell responses to viral infection

A

-Expand dramatically during the first 1-2 weeks post-infection
-Directly kill infected cells
-Make lots of antiviral cytokines such as IFN-gamma and TNF-alpha
-Memory cell capacity for long-term protection
-Rapid effector functions and high numerical expansion

51
Q

Distinguish between endogenous and exogenous antigens and which T cells recognize them, AND which MHC class presents the antigen to the T cells

A

Endogenous: Produced within the cell, such as a virus or intracellular bacteria producing proteins in the cytosol. Tc cells recognize on MHC-I

Exogenous: Come from outside of cell and then taken up through phagocytosis. Th cells recognize on MHC-II

52
Q

What are regulatory T cells?

A

Differentiate from helper T cells that suppress immune response

53
Q

What are innate lymphoid cells (ILCs)? Function? Example of ILC?

A

Lymph-like cells that produce cytokines and perform similar functions to lymphs, BUT do NOT express TCRs!

Function to provide early defense against infectious pathogens, recognize stress/damaged host cells, and eliminate cells

Example of ILC is the NK cell

54
Q

Describe NK cells

A

Respond to viral infections. Patients with selective NK deficiencies have recurrent, severe viral infections. Destroy target cells through a mechanism called “cytotoxic reaction.” Will kill virally infected cells (because of lack of self MHC-I receptor)

55
Q

Why do B lymphs have an unfavorable image?

A

Because while they can produce antibodies helpful to the host, they can also produce harmful anti-self antibodies

56
Q

List general B cell roles

A

-Natural immunity and major IgM source
-Host protection
-Clearance of apoptotic cells
-Possible negative-selection of self-reactive B cells
-Response to stress-induced antigens

57
Q

Which cell surface antigen do B cells express? What is a caveat?

A

CD19
Caveat is that plasma cells lose CD19.

58
Q

Which cell surface antigen do B cells NOT express? Which cell expresses it instead?

A

CD3. T cells express it

59
Q

List and briefly describe B cell subsets (include CD marker if applicable)

A

B1 cells: Express CD5. Function to respond to a number of common pathogens and occasionally generate autoantibodies

B2 cells: Account for MOST adult B cells, generate greater diversity of Ag receptors, and respond well to T-dependent Ag

MZ (marginal zone) B cells: rapid responses to blood-borne pathogens and T-independent Ab

60
Q

In which disease states do you see an increase in plasma cells?

A

-viral disease (rubella mononucleosis)
-allergies
-chronic infections
-collagen diseases
-dyscrasias (e.g., multiple myeloma, Waldenstrom macroglobulinemia)

61
Q

How does total T cell peripheral blood population change throughout adulthood?

A

Total T cell population remains relatively stable in the peripheral blood throughout adulthood

62
Q

How does T cell subset composition change as we age?

A

Older adults demonstrate a reduction in suppressor T cells and an increase in CD4+ T cells

63
Q

How does immunologic response correlate with age? Examples?

A

They correlate because any reduction in T cells is associated with pathology. For example, T cell deficits result in delayed hypersensitivity and impaired cellular immunity. A decrease in helper T cells leads to impaired humoral response in older adults

64
Q

List the 3 types of immunologic disorders

A
  1. Primary processes
  2. Acquired/Secondary processes
  3. Third category
65
Q

Define Primary Processes of immunologic disorders

A

Dysfunction in the immune organ itself (sounds congenital to me)

66
Q

Define acquired/secondary processes of immunologic disorders

A

Disease or therapy causing an immune defect

67
Q

Define the “Third Category” of immunologic disorders

A

Diseases mediated through immune mechanisms. This is another way of saying “autoimmune”

68
Q

List and give examples of allergic/hypersensitivity reactions

A
  1. Allergic hypersensitivity (pollen, food, drugs, mold)
  2. Contact hypersensitivity (poison ivy, nickel, cosmetics
  3. Autoimmune disease (SLE, RA, Grave’s disease, pernicious anemia)
69
Q

Gaucher disease is common in which group of people?

A

Ashkenazi Jews

70
Q

Name the cell surface marker of hematopoietic stem cells (HSCs)

A

CD34+

Clinical Immunology (14 decks)

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