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STEP 1 > 05a: Immunology > Flashcards

05a: Immunology Flashcards

1
Q

(Primary/secondary) lymph nodes follicles have pale central germinal centers and are (active/dormant).

A

Secondary; active

Primary follicles are dense and dormant

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2
Q

Viral infection: which part(s) of lymph node would you expect to enlarge?

A

Paracortex (T-cell zone), between follicles and medulla

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3
Q

Trachea and esophagus drain to (X) lymph nodes.

A

X = mediastinal

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4
Q

Which structure(s) drain to axillary lymph nodes?

A

Limbs, breast, skin above umbilicus

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5
Q

Celiac nodes drain up to (X) part of GI tract. SMA drain up to (Y) part. IMA drain up to (Z) part.

A 
X = upper duodenum
Y = splenic fixture (colon)
Z = upper rectum
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6
Q

Lower rectum to anal canal (above pectinate line) drains to (X) lymph nodes. And anal canal below pectinate line to (Y) nodes.

A 
X = Internal iliac
Y = superficial inguinal
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7
Q

Vagina and cervix drain to (X) lymph nodes. Uterus drains to (Y) lymph nodes. Ovaries drain to (Z) lymph nodes.

A 
X = internal iliac
Y = Z = para-aortic
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8
Q

Kidneys drain to (X) lymph nodes. Bladder to (Y) lymph nodes.

A 
X = para-aortic
Y = internal iliac
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9
Q

Nearly all skin below umbilicus drains into (X) lymph nodes. The exception is (Y) part of leg.

A 
X = superficial inguinal
Y = posterior calf and dorsolateral foot (drain into popliteal nodes)
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10
Q

Prostate drains into (X) lymph nodes.

A

X = internal iliac

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11
Q

T/F: R lymphatic duct only drains R side of body above diaphragm.

A

True - thoracic duct (L) drains everything else

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12
Q

Why are (lymphopenia/lymphocytosis) and (thrombopenia/thrombocytosis) consequences of splenectomy?

A

Lymphocytosis and thrombocytosis - due to loss of sequestration/removal by spleen

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13
Q

Periarteriolar lymphoid sheath (PAL) is found in which structure?

A

Spleen - the T cell zone

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14
Q

Which structure in spleen is the site for APC capture of blood-borne antigens for lymphocyte recognition?

A

Marginal (outermost) zone of follicle

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15
Q

Thymomas are associated with which two diseases?

A
  1. Myasthenia Gravis

2. SVC syndrome

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16
Q

In which genetic syndromes is the thymus hypoplastic?

A
  1. DiGeorge

2. SCID

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17
Q

MHC I protein structure: (X) number of (short/long) chains.

A

X = 2

ONE short, ONE long (for MHC ONE)

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18
Q

MHC II protein structure: (X) number of (short/long) chains.

A

X = 2

TWO long/equal-length chains for MHC TWO

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19
Q

MHC (I/II) is more exclusive, only present on (X) cells.

A

II
X = APCs

(MHC I on all nucleated cells)

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20
Q

MHC I: (exogenous/endogenous) Ags are presented to (X) cells.

A

Endogenous (viral, cytosolic proteins)

X = CD8 T cells

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21
Q

MHC II: (exogenous/endogenous) Ags are presented to (X) cells.

A

Exogenous (bacterial proteins)

X = CD4 T cells

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22
Q

MHC I: antigens loaded onto receptor in (X).

A

X = RER (after delivery through transporter, TAP)

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23
Q

MHC II: antigens loaded onto receptor in (X).

A

X = endosome (after acid environment releases CLIP protein that blocks MHC II binding site)

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24
Q

Beta2 microglobulin is associated with MHC (I/II). And invariant chain with MCH (I/II).

A

I;

II (blocks MHC II binding site via CLIP until proper Ag present)

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25
Q

Which diseases associated with HLA B27?

A 
Seronegative arthropathis ("PAIR")
Psoriasis, Ankylosing spondylitis, IBD-associated arthritis, Reactive arthritis
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26
Q

Which diseases associated with HLA DQ2/DQ8?

A

Celiac disease

“I 8 2 much gluten at DQ (Dairy Queen)”

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27
Q

Multiple sclerosis associated with which HLA subtype?

A

DR2

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28
Q

SLE associated with which HLA subtype?

A

DR2/DR3 (“2-3 for SLE”)

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29
Q

DM I associated with which HLA subtype?

A

DR3/DR4

Note: so is Addison’s disease

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30
Q

Hashimoto’s associated with which HLA subtype?

A

DR2/DR4

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31
Q

Pernicious anemia associated with which HLA subtype?

A

DR5

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32
Q

Rheumatoid arthritis associated with which HLA subtype?

A

DR4

“4 walls in a rheum”

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33
Q

Candida superficial infection (ex: oral/esophageal, cutaneous, vulvovaginitis) is prevented by which members of immune system?

A

T lymphocytes (hence HIV or other low T count conditions cause superficial candidiasis)

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34
Q

Candidemia or other forms of disseminated candidiasis is prevented by which members of immune system?

A

Neutrophils! (hence more likely in chemo/neutropenic patients)

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35
Q

Which cytokines enhance NK cell activity?

A

IL2, IL12, IFNa, IFNb

36
Q

Target cell with (present/absent) MHC (I/II) will be killed by NK cell.

A

Absent

MHC I

37
Q

CD(X) on NK cell can activate it when binding to (Y) region of Ig.

A 
X = 16
Y = Fc
38
Q

T/F: T cells responsible for both acute and chronic cell organ rejection.

A

True

39
Q

Helper T cell can become TH1 differentiated with help of (X) cytokines.

A

X = IL-12, IFN-gamma

40
Q

Helper T cell can become TH2 differentiated with help of (X) cytokines.

A

X = IL-2, IL-4

41
Q

Helper T cell can become TH17 differentiated with help of (X) cytokines.

A

X = IL-6, TGF-beta

42
Q

Helper T cell can become Treg differentiated with help of (X) cytokines.

A

X = TGF-beta

43
Q

Thymus: self-antigens found in tissues are expressed during negative selection by the action of (X). Deficiency of (X) leads to which syndrome?

A

X = AIRE (autoimmune regulator)

Autoimmune polyendocrine syndrome 1

44
Q

TH1 cell inhibits TH2 differentiation by secreting (X). And TH2 inhibits TH1 differentiation by secreting (Y).

A 
X = IFN-gamma
Y = IL-4, IL-10
45
Q

Main action of TH1-differentiated T cells

A

Activate macrophages and cytotoxic T cells

46
Q

Main action of TH2-differentiated T cells

A

Recruit eosinophils (parasite defense) and IgE production by B cells

47
Q

T/F: NK cells and cytotoxic lymphocytes kill via same mechanism.

A

True - perforin and granzyme release causes cell apoptosis

48
Q

T-regulatory cells produce (X) cytokines and are identified by expression of which receptors?

A

X = anti-inflammatory (IL-10, TGF-beta)

CD3, CD4, CD25, FOXP3

49
Q

Which costimulatory signal is required for T cell activation? And for B cell activation/class switching?

A

T cell: CD28 (on helper/cytotoxic T cell) with B7 (on APC)

B cell: CD40 (on B cell) with CD40L (on helper T Cell)

50
Q

Three steps/components of generating antibody diversity (independent of antigen)

A
  1. VDJ (heavy chain) and VJ (light chain) gene recombination
  2. Random NT addition to DNA by TdT during recombination
  3. Random heavy and light chain combinations
51
Q

Two steps/components of generating antibody specificity (dependent on antigen)

A
  1. Somatic hypermutation and affinity maturation (in variable region of Ab)
  2. Isotype switching (of Ab constant region)
52
Q

T/F: IgG is the isotype that is most abundant in serum and produced the most overall.

A

False - most abundant in serum, but IgA is the isotype produced most (despite low serum conc)

53
Q

If you could test for antibodies in your tears, which isotype would you expect to find?

A

IgA (released into secretions like saliva, tears, mucus, breast milk)

54
Q

The antibody receptor on B cells that recognizes antigen is which isotype?

A

IgM (monomer form)

55
Q

Vaccination: antigens (containing/lacking) (X) component often require boosters/adjuvants. Why?

A

Lacking;
X = peptide (ex: LPS on G- bac)

No protein component means can’t be presented on MHC (thymus-independent; weakly immunogenic)

56
Q

T/F: NK cells kill by cell lysis.

A

False - perforins make holes in target cell, granzymes enter and induce APOPTOSIS

57
Q

Major component of adaptive immunity against Giardia is:

A

IgA (deficiency predisposes to chronic giardiasis)

58
Q

Acute phase reactants are produced by (X) and notably induced by (Y) cytokine.

A 
X = liver
Y = IL-6
59
Q

Iron (absorption/release/sequestering) is increased in state of inflammation due to action of which acute-phase reactant(s)?

A

Absorption and release are decreased (via hepcidin); sequestering into cells is increased (via ferritin)

60
Q

Hepatic synthesis of which two key proteins is down-regulated in response to inflammation?

A
  1. Albumin (to conserve AA for acute-phase reactants)

2. Transferrin (to keep iron sequestered in macrophages)

61
Q

List the 3 complement pathways and the activators of each

A
  1. Classic: IgG, IgM (“GM makes classic cars”); Ag-Ab complexes
  2. Alternative: microbe surface molecules
  3. Lectin: mannose/sugars on microbe surface
62
Q

The three complement pathways find common ground/converge on (X).

A

X = C3 (cleavage into C3a, C3b)

63
Q

Complement: C4b2b is also known as (X) and is formed from which complement pathway(s)?

A

X = C3 convertase

Lectin (C4b) plus Classic (C2b) pathways

64
Q

Complement: C3bBb is also known as (X) and is formed from which complement pathway(s)?

A

X = C3 convertase

Alternative (C3b) pathway (plus B cleavage product into Bb)

65
Q

Complement: C4b2b3b is also known as (X).

A

X = C5 convertase (can also arise from C3bBb3b product)

66
Q

MAC complex is composed of which complement factors?

A

C5b-C9

67
Q

Which complement factors are responsible for anaphylaxis?

A

C3a, C4a, C5a (“a” for “anaphylaxis”)

68
Q

Which factor deficiency is associated with severe, recurrent pyogenic sinus/resp infections as well as high susceptibility to type III HS rxns?

A

C3 deficiency (immune complexes can’t be cleared)

69
Q

Low C1 esterase inhibitor is diagnostic for (X). The pathogenesis of this disease is centered around (activation/inhibition) of (Y).

A

X = hereditary angioedema (AD inheritance)

Unregulated activation of kallikrein (high bradykinin)

70
Q

IL-1 function(s)

A
  1. Fever, inflammation
  2. Endothelial activation to express adhesion molecules
  3. Chemokine secretion

“Hot (IL-1) T-bone stEAK”

71
Q

IL-2 function(s)

A

Stimulates growth of T cells (as well as NK cells)

“Hot T (IL-2)-bone stEAK”

72
Q

IL-3 function(s)

A

Stimulates bone marrow (growth/differentiation of stem cells; similar to GM-CSF)

“Hot T-bone (IL-3) stEAK”

73
Q

IL-4 function(s)

A

Induces TH2 differentiation and B cell growth; IgE (and IgG) class switch

“Hot T-bone stE(IL-4)AK”

74
Q

IL-5 function(s)

A

Growth/differentiation of B cells and IgA class switch; eosinophil growth/differentiation

“Hot T-bone stEA(IL-5)K”

75
Q

IL-6 function(s)

A

aKute phase reactants

“Hot T-bone stEAK(IL-6)”

76
Q

PMN phagolysosome: first key step is converting (X) to (Y) with which enzyme?

A 
X = O2
Y = O2- (free radical)

NADPH oxidase (deficient in chronic granulomatous disease)

77
Q

PMN phagolysosome: second key step is converting (X) to (Y) with which enzyme?

A 
X = O2- (free radical)
Y = H2O2

superoxide dismutase

78
Q

PMN phagolysosome: Bleach can be formed via which reaction/enzyme?

A

H2O2 combined with Cl (enzyme: myeloperoxidase)

79
Q

Green sputum: what gives it the color?

A

Myeloperoxidase

80
Q

(X) enzyme in neutrophil converts H2O2 to H2O by (oxidizing/reducing) glutathione. What does it require for proper function?

A

X = Glutathione peroxidase
Oxidizing

Selenium

81
Q

Glutathione reductase work by simultaneously (oxidizing/reducing) (NADP/NADPH). The reaction requires (X) for proper function.

A

Oxidizing; NADPH

X = riboflavin

82
Q

IFN-alpha and beta are secreted by (X) cells and act on (Y).

A 
X = virus-infected cells ("INTERFERe with viruses")
Y = local uninfected cells ("prime them" by inducing them to decrease protein synthesis and upregulate MHC expression)
83
Q

Macrophages express CD(X) receptor for PAMPs like bacterial LPS.

A

X = 14

84
Q

T and B cells become anergic when:

A

Exposed to antigen without co-stimulatory signal

85
Q

Superantigens, such as those produced by (X) bacteria, cause massive release of cytokines by which mechanism?

A

X = S. aureus, S. pyogenes

Cross-link beta region of TCR to MHC II on APCs (can activate any CD4 T cell)

86
Q

T/F: Shock caused by N. meningitides is mediated by T-helper cells.

A

False - endotoxins/LPS directly stimulate macrophages by binding TLR (CD14); no T cells involved

STEP 1 (21 decks)

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