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Board/First Aid > General Immuno > Flashcards

General Immuno Flashcards

1
Q

Location of T cells in the sinusoids of the spleen.

A

Scattered in the White Pulp

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2
Q

Location of B cells in the sinusoids of the spleen.

A

Germinal Centers in the White Pulp

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3
Q

4 major infectious organisms more common with asplenia

A 
Encapsulated organisms (lower IgM means no C3b production)
Salmonella
Strep pneumo
H. flu
Neisseria m.
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4
Q

What branch of immunity is complement a part of?

A

Innate

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5
Q

What are HLA-A, HLA-B, and HLA-C?

A

MHC I receptors

  • they bind to TCR with co receptor CD 8 on T cells
  • present on all nucleated cells
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6
Q

What are HLA-DR, HLA-DP, HLA-DQ?

A

MHC II receptors

  • bind TCR and co-receptor CD4 on T cells
  • present on cells that serve as APCs
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7
Q

What is HLA-A3 associated with?

A

Hemochromatosis

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8
Q

What is HLA-B27 associated with?

A

Psoriasis, Ankylosing Spondylitis, IBD, Reiters Syndrome

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9
Q

What is HLA-B8 associated with?

A

Graves Disease

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10
Q

What is HLA-DR2 associated with?

A

MS, SLE, hay fever, Goodpastures

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11
Q

What is HLA-DR3 associated with?

A

DM type 1

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12
Q

What is HLA-DR4 associated with?

A

RA and DM type 1

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13
Q

Where do positive and negative selection of T cells occur in the thymus?

A

Positive: cortex, T cells must have TCR that bind MHC
Negative: medulla, T cells that have TCR that bind self antigens are eliminated

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14
Q

Mechanism of CD4 cell activation

A
  1. APC “eats” foreign material, digests it, puts it on MHC II
  2. MHC II recognized by TCR on CD4 on helper T cells
  3. Co-signal of B7 (on APC) and CD28 (on T cell) must also bind
  4. CD4 cell produces cytokines (IL-2 ) to activate CD8 cells
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15
Q

2 Mechanisms of CD8 activation

A
  1. Cell infected by viral or bacterial pathogen presents material on MHC I
  2. MHC I binds TCR (along with CD8) on cytotoxic T cells

Another mechanism is IL-2 released from CD4 T cells binds the IL-2 receptor on CD8 T cells to activate them.

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16
Q

Mechanism of B cell activation

A
  1. CD4 T cell releases IL-4, IL-5 and IL-6 to induce B cell differentiation and produce Abs
  2. CD40 (B cells) binds CD40L (T cell) as a Co-stimulation
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17
Q

Difference between Th1 and Th2 CD4 cells

A

Th1

  • CMI
  • secretes IL-2, INF-gamma
  • inhibited by IL-10

Th2

  • humoral immunity
  • secretes IL-4, IL-5, IL-10
  • inhibited by INF-gamma
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18
Q

Portion of which two Abs induce classic complement pathway?

A

Fc portion of IgM and IgG

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19
Q

Abs on the surface of Mature B cells

A

IgM and IgD

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20
Q

Ab that crosses the placenta to give immunity to neonates

A

IgG

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21
Q

Ab passing thru breast milk

A

IgA

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22
Q

Ab that forms a pentamer in circulation

A

IgM

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23
Q

Ab that is used in parasite infections and allergies

A

IgE

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24
Q

Complement protein that serves for opsonization

A

C3b

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25
Q

Complement proteins that serve in anaphylaxis

A

C3a and C5a

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26
Q

Complement protein that serves in neutrophil chemotaxis

A

C5a

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27
Q

Complement protein that functions to clear immune complexes

A

C3b

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28
Q

Condition and contraindicated drugs in C1 esterase inhibitor deficiency

A

Hereditary angioedema

-no ACE-Is

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29
Q

2 pyrogenic cytokines secreted by macrophages

A

IL-1

IL-6

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30
Q

Chemotactic cytokine secreted by macrophages

A

IL-8

31
Q

Cytokine secreted by macrophages that induces Th1 formation and activates NK cells

A

IL-12

32
Q

Cytokine secreted by macrophages that mediates septic shock

A

TNF-alpha

33
Q

Cytokine secreted by all T cells that induces bone marrow growth and differentiation

A

IL-3

34
Q

2 mediators from Th1 cells and the functions

A

IL-2: growth and differentiation of cytotoxic T cells

INF-gamma: activates macrophages, suppresses Th2 cells

35
Q

4 mediators from Th2 cells and the functions

A

IL-4: induces IgE production in B cells
IL-5: induces IgA production in B cells
IL-6: pyrogen
IL-10: inhibits inflammation, suppresses Th1 formation

36
Q

Function of INF-alpha and beta

A

Inhibit viral protein synthesis

37
Q

Function of INF-gamma

A

induces MHC I and II expression

38
Q

B cell receptor that binds EBV

A

CD21

39
Q

Unique receptor on NK cells

A

CD56

40
Q

Mechanism of Superantigens causing shock

A

Ag facilitates a very strong binding “outside the normal Ag site” of the TCR (w/ CD4) and MHCII. Causing a prolonged binding which induces release of:
IL-1, IL-6, and TNF-alpha from macrophages

41
Q

Mechanism of LPS endotoxin causing shock

A

LPS binds CD14 on macrophages induces IL-1, IL6, and TNF-alpha release

42
Q

Mechanism of passive immunity and a big example

A

Receive pre-formed Abs

  • IgA in breast milk
  • rapid acting but not long lasting
43
Q

Mechanism of active immunity

A

Actual exposure to foreign antigens causes the body to slowly produce natural Abs to the specific Ag

44
Q

Mechanism of Type I HS reaction

A

Allergen stimulates IL-4 release from Th2 cells. Induces B cells to make IgE.

  • Fc portion of IgE binds to mast cells and basophils
  • second exposure causes mast cell degranulation
45
Q

Antibodies involved in Type II HS reactions

A

IgM and IgG

46
Q

Antibody involved in Type III HS reactions

A

IgG

-binds and Ag which activates complement (3 things in Type III)

47
Q

What are 4 general categories of Type IV HS reactions?

A

T lymphocytes
Transplants
Tuberculosis skin test
Touching (contact dermatitis)

48
Q

Anti dsDNA Abs

A

SLE

49
Q

Antimitochondrial Abs

A

Primary biliary cirrhosis

50
Q

Anticentromere Abs

A

Scleroderma CREST

51
Q

Anti-desmoglein

A

Penphigus Vulgaris

52
Q

Anti-Ro

A

Sjogren Syndrome (also Anti-SS-A)

53
Q

c-ANCA

A

Wegener Granulomatosis

54
Q

Anti-IgG

A

RA (anti Rheumatoid factor)

55
Q

Anti-histone

A

Drug Induced Lupus

56
Q

Anti-topoisomerase I

A

Scleroderma (diffuse)

57
Q

Anti-basement membrane

A

Goodpasture Syndrome

58
Q

Antimicrosomal or Antithryoglobulin

A

Hashimotos

59
Q

Anti-La

A

Sjogren Syndrome (also Anti-SS-B)

60
Q

anti-Smith Abs

A

SLE

61
Q

What is the general rule about T cells deficiency and B cell deficiency

A

T cell def. produce more fungal and viral infections

B cell def. produce more recurrent bacterial infections

62
Q

Patient presents with recurrent bacterial infections. What is the gene mutated in this immunodeficiency?

A

Bruton Agammagobulinemia

  • Brutons Tyrosine Kinase
  • needed for B cell maturation
63
Q

Patient presents with severe pyrogenic infection early in life.

A

Hyper-IgM Syndrome

  • Defective CD40L (Th2) or CD40 (B cells)
  • receptors needed for class switching
64
Q

Young patient presents with tetany, recurrent fungal infections, and great vessel defects. What is the embryology behind this condition?

A

DiGeorge Syndrome (CATCH-22)

  • mutation on chromosome 22q11
  • failure of the 3rd and 4th pharyngeal pouches
  • Cardiac Abnormalities (T of F)
  • Abnormal Facies
  • Thymic Aplasia
  • Cleft Palate
  • Hypocalcemia (due to low PTH and no Parathyroids)
65
Q

Patient presents with recurrent staph infections, also has his baby teeth at 14 years of age and eczema.

A

Hyper IgE syndrome (Job Syndrome)

-Th cells fail to secrete IFN-gamma for neutrophil chemotaxis

66
Q

Patient presents early in life with recurrent viral, bacterial, fungal, and protozoal infecitons. What is the mechanism for this condition?

A

SCID

  • defective IL-2 receptor and/or adenosine de-aminase deficiency (can’t produe MHC II)
  • inability to produce B and T cells
67
Q

Patient presents with recurrent mucosal infections, spider angiomas, and difficulty walking.

A

Ataxia Telangeictasia

-IgA deficiency

68
Q

Patient presents with thrombocytopenic purpura, recurrent infections, and eczema.

A

Wiskott Aldrich Syndrome

-low IgM

69
Q

Patient presents with recurrent bacterial infections without pus formation. Delayed umbilical cord separation.

A

Leukocyte Adhesion Deficiency

-defect in integrins that bind CD18

70
Q

Nitroblue tetrazolium dye doesn’t turn blue

A

Chronic Granulomatous Disease

  • defect in NADPH oxidase
  • no ROS produced to fight bacteria
  • catalase positive organisms
71
Q

What is a syngeneic graft?

A

Graft from identical twin

72
Q

Mechanism of Hyperacute graft rejection

A

Type II HS reaction of preformed Abs

-cytotoxic, occlusion of graft vessels and ischemia

73
Q

Mechanism of Graft vs. Host disease

A

Type IV

-graft from immunocompetent patient given to IC host and T cells attack host

74
Q

MOA of cyclosporine

A

Prevents calcineurin formation in T cells. This is a molecular signaling molecule needed for IL-2 production
-used for grafts and gout

Board/First Aid (6 decks)

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