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FMS Week 8 (also some 7) Immunology > Immunology: Case Studies 1 > Flashcards

Immunology: Case Studies 1 Flashcards

1
Q

What is the immune role of the thymus?

A)NK cell development and selection

B) B lymphocyte development and selection

C) T lymphocyte development and selection

D) Monocyte development and selection

E) Neutrophil development and selection

A

C) T lymphocyte development and selection

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2
Q

Patient with digeorge syndrome

Numerous severe viral infections and fungal infections

cleft pallette

wide separated low ears

A

NO THYMIC SHADOW

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3
Q

Development if T cells in the thymus

A

Double negative T cells do not express CD4 or 8

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4
Q

What best describes T lymphocyte selection in the thymus> After TCR rearrangement comes

A) only negative selection of TLR

b) only positive selection of MHC
c) positive selection and negative selection os TLR
d) positive selection on TLR; negative selection on MHC
e) positive and negative selection on MHC

A

e) positive and negative selection on MHC

TLR is toll like receptor. They are involved in sensing a pathogen. Dont play a role in T cell development

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5
Q
A

Positive selction of T cells

Double positive thymocytes

If receptor binds self MHC class I it will be a CD8 T cell

If binds self peptide MHC class II it will become CD4T cell

Negative selection happens to get rid of. cells that react to strongly to self peptides/antigen

If binding affinity high, will not be viable

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6
Q
A

Negative selection of T cells to kill off cells with high affinity for self antigen

moderate or low binding affinity and cell lives

high affinigty (tight binding) and cell dies

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7
Q
A

Blue part is produce TCR and then positive selction

orange part is nagative selection

Mature self-restricted, slef tolerant, single positive CD4 or CD8 T cells leqave the thymus in blood vessels

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8
Q

What are the main effector functions of T lymphocytes

a) CD4 cytotoxic ; CD8 secrete cytokines
b) CD4 pagocytic; CD8 secrete cytokines
c) CD4 secrete cytokines; CD8 cytotoxic
d) CD4 secrete cytokines; CD8 pagocytic

A

c) CD4 secrete cytokines; CD8 cytotoxic

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9
Q
A

Helper T cell secreting cytokines after microbial antigen presentation by APC which activates macrophages, inflammation, and activation (priliferation and differentiation) of T and B lymphocytes

cytotoxic T lymphocyte
Infected cell expressing microbial antigen
Ag presentation by MHC class I, then killing of infected cell

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10
Q

The child with digeorge has no detectable thymus (ie no T cells). What innate defense mechanisms are still present to kill viruses?

a) IFN-α and IFN-ß; natural killer (NK) cells
b) phagocytic cells; B lymphocytes
c) pagocytic cells; CD8 lymphocytes
d) Interleukin-2 (IL-2); eosinophils

A

a) IFN-α and IFN-ß; natural killer (NK) cells

IFN are antiviral

NK cells recognise and kill infected cells
these cells have downregulated MHC class I

Can not be B. phagocytic cells usually not viral killers

B lymphocytes are part of the adaptive immune response, not innate. They also need helper T cells to class switch and activate B cells

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11
Q

IFN-α and IFN-ß

action against viruses

classificiation

A

Antiviral activity
activation of NK cells
inhibits viral replicaiton

Innate

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12
Q

NK cells

action against viruses:

Classification:

A

Lysis of infected cells

innate

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13
Q

CD4 T cell

action against viruses:

classification

A

Produce cytokines to help B cells and CD8 T cells

Adaptive

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14
Q

CD8 T cell

action against viruses:

classification

A

Lysis of infected cell; produce cytokines to help NK cells become cytotoxic

adaptive

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15
Q

B cell

Action against viruses

Classification

A

Produce antibody; neutralization, opsonization for ADCC

ADCC = antibody dependent cellular cytotoxicity. The lysis of an infected cell

Adaptive

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16
Q

DiGeorge

A

22q11

THYMUS DOES NOT DEVELOP

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17
Q

Bare lymphocyte syndrome

A

Child with history of bacterial, viral, and fingal infections

long episodes of D

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18
Q

Bare lymphocyte syndrome lab tests

A

CBC and differential: normal total number of neutrophils, monocytes, lymphocytes, eosinophils, and basophils

Antibody titers for immunization antigens were negligible

Nitroblue tetrazolium (NBT) test showed normal respiratory bursts after phagocytosis (ie phagocytes can kill)

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19
Q

Bare lymphocyte syndrome

Based on the infection history and lack of antibody responses, where do you suspect the defect to be?

Natural killer (NK) cells

Lymphocytes

Neutrophils

Eosinophils

A

Lymphocytes

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20
Q

What antibodies do

A
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21
Q

Which cell population helps B cells make antibody?

NK cells

CD4 lymphocytes

CD8 lymphocytes

Macrophages

A

CD4 lymphocytes

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22
Q
A
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23
Q

Bare lymphocyte syndrome

Flow cytometry shows severe CD4 lymphopenia. Where do suspect the defect?

Complement proteins expression

MHC class I expression

MHC class II expression

TLR expression

A

MHC class II expression

Why would lack of MHC II mean no CD4 cells? Posisive selection

None can come out of the thymus to periphery

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24
Q
A

No CD4 cells = No B cell help

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25
Q

BLS is a rare autosomal disorder caused by genes that control expresison of what

A

MHC class II.

MHC class II is not expressed on APCs

Tx: IV immunoglobulin, bone marrow transplant

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26
Q

In addition to B cells, what other immune cells express MHC class II

a) dendritic cells and macrophages
b) NK cells and neutrophils
c) basophils and eosinophils
d) CD4 and CD8 lymphocytes

A

a) dendritic cells and macrophages

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27
Q
A
28
Q

Which cell surface molecule is responsible for presenting viral antigen derived from virus infecting a cell?

CD4

CD8

MHC class I

MHC class II

TLR

A

MHC Class I

Protein being synthesized endogenously.

MHC Class I

29
Q

In humans, what are the MHC genes known as?

H-2

B

HLA

ABO

ABD

A

HLA

30
Q

Which type of antigen is processed for presentation by MHC molecules?

polysaccharides

nucleic acid

protein

glycolipid

carbohydrates

A

PROTEIN

31
Q

Development of protection in a primary adaptive immune response to a T dependent antigen takes approximately how much time?

30-120 mins

6-24 hours

1-4 days

1-3 weeks

2-6 months

A

1-3 weeks

32
Q
A

Increase in memory cells after priming means that the secondary response is fater and greater

33
Q

LAD-1

Leukocyte adhesion deficiency

A

8 year old F with recurrant necrotic infections to the arms and legs.

34
Q

LAD-1 Lab tests

A

CBC diff: normal

Complement levels and function: normal

Nitroblue tetrazolium (NBT) test: normal

Serum Ig (total levels) : normal

Antibody titers for vaccine antigens: normal

35
Q

What cell type is rapidly recruited to the site of a bacterial infection in the skin?

eoinophils

neutrophils

basophils

NK cells

A

Neutrophils

36
Q

What role do neutrophils play in an immune response against a pathogen?

a) antigen presentation to CD4 lymphocytes
b) induce B lymphocytes to make antibody
c) phagocytose and kill foreign pathogens
d) activate NK cells

A

c) phagocytose and kill foreign pathogens

37
Q

Neutrophil function and what they express

A

Neutrophils stored in bone marrow and are released when needed to fight infection

They travel to and enter the infected tissue wher they engulf and kill bacteria. They die in the tissue and are engulphed and degraded by macrophages

Neutrophils express receptors for many bacterial and fungal constituents

Neutrophils bind bacteria, engulf them, and destroy them with the toxic components of the neutrophil granules

38
Q

Neutrophils were prominent in the patient’s blood and were functional, but were not observed at the site of the infection. What molecule is most likely defective?

pattern recognition receptor

complement

MHC class I

Integrins

A

INTEGRINS

39
Q

The child has been diagnosed with leukocyte adhesion deficiency 1 (LAD-1) due to the defect in CD18 (a component of beta-2 integrin/LFA-1

A

If you look at the picture, you can see that LFA-1 is important in binding and rolling for neutrophil adhesion and entering into tissue.

Thus cell can not get into tissue and can not fight infection

40
Q

LAD 2

A

Trafficking defect due to defects in carbohydrates present on the leukocyte cell surface

Carbohydrates are the ligands for P selectin and E selectin

Cell rolloing to slow down the leukocyte does not occur

41
Q

What is one immune function of the spleen

a) capture lymphatic borne antigen
b) capture blood borne antigen
c) capture mucosal associated antigen

A

b) capture blood borne antigen

lymphatic borne antigen is captured in the LN

42
Q

What is the function of the red pulp?

Remove aged or abnormal RBCs

Activate eosinophils

Generate antibodies

Activate NK cells

A

Remove aged or abnormal RBCs

(white pulp is analogous to LNs)

43
Q
A

Howell-Jolly bodies in blood smear. Inclusions are formed by the retention of nuclear remnants in red cells which are usually removed by spleen

44
Q

What is the function of the white pulp?

Mast cell activation

Secrete complement factors

Interactions between B and T lymphocytes

Activate NK cells

A

Interactions between B and T lymphocytes

45
Q

Ways antibodies eliminate pathogens

A

neutralization

opsonization

46
Q

Neutralization

A

Ab binds to pathogen in a way that inhibits pathogen growth, replication, or interaction with human cells; Ab binds to toxin to inhibit activity

47
Q

Opsonization

A

coating of pathogen with Ab/ Ab+ complement for efficient phagocytosis

48
Q
A

Ways that Abs eliminate pathogens

neutralization and opsonization

49
Q

Most common and rapidly progressing infections after splenectomy are

A

streptococcus pneumoniae and haemophilus influenzae

Encapsulated pathogens that can enter the bloodstream

eliminated by innate and adaptive immune respinses in the spleen

50
Q

Asplenic patients are given what as treatment

A

antibiotic prophylaxis

51
Q

Complex immunodeficiency

A

31 year old F with nasal perforation and ulcerated brown-violet skin lesions

Hx TB

52
Q

Complex immunodeficiency labs

A

Leukocytes : normal

Lymphocytes: normal

T cells (CD3+): Normal

CD4 T cells: Normal

CD8 T cells: Absent (αß)

CD4- CD8- γδ T cells: High

B cells: normal

IgG: Low

Other Ig: Normal

Note γδ T cells are a specialized calss of T cells that are not selected in the thymus and are not MHC restricted. They are resident to epithelial surfaces.

53
Q

Complex immunodeficiency

Where do you suspect the defect?

B lymphocyte development and selection

T lymphocyte development and selection

Monocyte development and selection

Neutrophil development and selection

A

T lymphocyte development and selection

54
Q

What mechanism of genetic recombination occurs in developing T lymphocytes that leads to the generation of the TCR

somatic hypermutation

somatic recombination

allele polymorphism

affinity maturation

A

Somatic recombination
AKA VDJ recomb.

Somatic hypermutation is the mutagenesis of B cells

Affinity maturation happens due to somatic hypermutation

55
Q

Complex immunodeficiency

Where do you suspect the defect?

MHC class I

MHC class II

RAG

CD3

A

MHC class I

56
Q
A

In complex immunodeficiency you do not have MHC class I and this can not self bind. Can not get CD8 cells bc of this.

57
Q

Complex immunodeficiency labs

FcRn (brambell receptor)

CD-1 expression

A

FcRn (brambell receptor): ABSENT

CD-1 expression: ABSENT

58
Q

FcRn AKA

A

FcRB (brambell receptor)

59
Q

What does FcRn (FcRB) do?

A

It helps increase the half life of IgG molecules

Responsible for maternofetal trandfer of IgG and normal IgG and albumin half-life

60
Q

Defective FcRn

A

Low IgG

61
Q
A

FcRB carries IgG acrosss endothelium into extracellular spaces

62
Q

Complex immunodeficiency:

Why the dysfunction in:

MHC class I

FcRn/FcRB

CD1

A

They all share the ß2-microglobulin as part of their structure

63
Q

Where do MHC class I molecules bind peptide?

Endosome compartment

Golgi apparatus

Endoplasmic reticulum

Cytosol

A

Endoplasmic reticulum

64
Q

MHC Class I pathway

A

Notice that TAP loads peptides onto MHC Class I.

TAP deficiency can also lead to lack of MHC class I expression

Mutations in TAP are the most common cause of MHC Class I deficiencies

65
Q

What cells express MHC class I?

Only DC, B cells, macrophages

All nucleated cells, but not DCs, B cells, macrophages

All nucleated cells

A

All nucleated cells

66
Q
A

Proteins processed by the endogenous vs the exogenous pathway

Endogenous- MHC class I expressed on nucleated cells
Presents viral and tumor antigens
Exogenous- MHC class II expressed on limited number of cells (mainly DCs, macrophages, B cells) 
Presents viral, bacterial,fungal, and environmental antigens
67
Q

The pt with complex immunodeficiency was diagnosed with

B-2 microglobulin

A

Hypogammaglobulinemia and hypoalbuminemia due to lack of expression of FcRn/FcRB

Deficiency in clearing extracellular pathogens

No CD8 Tc cells in blood due to no MHC class I expression
deficiency in clearing intracellular pathogens

FMS Week 8 (also some 7) Immunology (9 decks)

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