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Rheum > 01a: Immunology > Flashcards

01a: Immunology Flashcards

1
Q

Type (I/II/III/IV) hypersensitivity reactions are mediated by Ab. What exactly is the culprit of disease?

A

I: Ab v. allergens
II: Ab v. tissue/cell Ag
III: Ig:Ag immune complexes

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2
Q

Type (I/II/III/IV) hypersensitivity reactions mediated by T cells, specifically (CD4/8/reg) T cells.

A

IV;

Both CD4 and CD8

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3
Q

T/F: Type III hypersensitivity reaction primarily caused by large immune complexes.

A

False - small complexes (large ones get cleared rapidly)

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4
Q

List the three requirements for disease to be truly “autoimmune”

A
  1. Immune rxn specific for self Ag
  2. Not simply secondary rxn to tissue injury
  3. Absence of well-defined cause of disease
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5
Q

Goodpasture syndrome: Ab directed against (X) with (Y)-mediated inflammation makes this Type (I/II/III/IV) HS reaction.

A 
X = non-collagenous proteins in basement membranes (in glomeruli and alveoli)
Y = Fc and complement

Type II

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6
Q

Systemic Lupus Erythematosus is a Type (I/II/III/IV) HS reaction with (X) antigens involved.

A

III;

X = nuclear

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7
Q

Insulin-resistant diabetes can be seen as Type (I/II/III/IV) HS reaction. What’s the Ag?

A

II;

X = Insulin receptor (Ab inhibits insulin binding)

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8
Q

Pemphigus vulgaris is Type (I/II/III/IV) HS reaction with (X) Ag involved. Skin vesicles (bullae) are formed as result of (Y)-mediated disruption of (Z).

A

II;
X = cadherin proteins in intercell junctions (of epidermal cells)
Y = protease
Z = intercellular adhesions

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9
Q

Post-strep glomerulonephritis is Type (I/II/III/IV) HS reaction with (X) Ag involved.

A

III;

X = Strep cell wall Ag (planted in glomerular BM)

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10
Q

Type IV HS reaction: how does (CD4/CD8) T cell cause tissue injury?

A

CD4: cytokine-mediated inflammation
CD8: direct killing

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11
Q

Immuno: Central tolerance develops in (X) and peripheral tolerance in (Y).

A 
X = thymus or marrow
Y  = periphery
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12
Q

Blood: ABO Ab are Ig(X) and Rh Ab are Ig(Y).

A 
X = M
Y = G
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13
Q

List the three requirements for T-cell negative selection (central tolerance) to occur.

A
  1. Location in thymus
  2. Self-peptide presented on APC
  3. T-cell with self-reactive T-cell receptor
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14
Q

What is/are the fate(s) of self-reactive T-lymphocyte during negative selection in thymus?

A
  1. Apoptosis

2. Become T-regs

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15
Q

T/F: Self-reactive T-lymphocyte directed against peripheral Ag can’t develop central tolerance since Ag not present in thymus.

A

False - AIRE (autoimmune regulator) stimulates expression of peripheral Ag on thymic medullary epithelial cells

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16
Q

What is/are the fate(s) of self-reactive B-lymphocyte during development of central tolerance?

A
  1. Receptor editing

2. Apoptosis

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17
Q

List the three mechanisms of peripheral tolerance.

A
  1. Anergy
  2. T-regs
  3. Activation-induced cell death
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18
Q

What’s the job of T-regs in the periphery?

A

Suppress APCs that present self-antigens

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19
Q

List the molecules essential for development of T-regs.

A
  1. IL-2 receptor

2. FoxP3 (TF)

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20
Q

List the general mechanisms by which T-regs work.

A
  1. Immunosuppressive cytokine secretion (IL-10, TGFb)

2. Competitively block co-stim molecule B7

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21
Q

T-Lymphocyte activation requires which receptor interactions with APC?

A
  1. Main signal: T-cell receptor with Ag-MHC

2. Co-stim signal: CD28 (T-cell) with B7 (APC)

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22
Q

Mechanisms of anergy (peripheral tolerance).

A
  1. Weak/absent co-stim molecule on peripheral APC

2. Inhibitory co-stim molecules expressed on lymphocytes

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23
Q

T/F: Either T or B cells may become anergic.

A

True

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24
Q

If co-stimulatory molecule on peripheral APC is weak/absent, how does this affect lymphocyte?

A

Anergy (functionally inactivated)

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25
Q

List the inhibitory co-stim molecules on T cells.

A

CTLA4, PD1

26
Q

List some examples of Type IV HS autoimmune diseases.

A
  1. Type I DM
  2. MS
  3. RA
  4. Crohn’s
  5. Guillain-Barré syndrome
27
Q

Ag in some anatomic sites are “hidden” and don’t elicit immune response unless (X). Give some examples.

A

X = traumatic injury exposes them

  1. Testes
  2. Brain
  3. Eye
28
Q

T/F: Genetic component of autoimmune diseases clearly exists.

A

True

29
Q

Several genes are associated with autoimmunity, and a common association is with (X) genes, thought to alter (Y) process.

A 
X = HLA
Y = negative selection
30
Q

List the general mechanisms by which infection may increase autoimmune disease symptoms.

A
  1. Increase co-stim molecules
  2. Molecular mimicry
  3. Cell damage
  4. More lymphocyte recruitment
31
Q

T/F: Autoimmune diseases tend to be symptomatically stable over time.

A

False - progressive (cell/tissue damage may uncover/create new Ag)

32
Q

Autoimmune diseases: epitope spreading refers to…

A

Spread of immune response to new/hidden Ag, beyond initial response

33
Q

T/F: Auto-antibodies, when detected, are always pathologic.

A

False - can be detected in large number of normal individuals (esp elderly)

34
Q

ANAs (antinuclear Abs) can be grouped into which categories?

A
  1. anti-DNA
  2. anti-histone
  3. Ab against non-histone proteins bound to RNA
  4. anti-nucleolar
35
Q

ANA Indirect Immunofluorescence test: a plate coated with (X) is exposed to (Y).

A 
X = nuclear Ag from human epithelial cell line
Y = patient serum (with auto-Ab)
36
Q

ANA Indirect Immunofluorescence test: FITC (fluorescein conjugated antiserum) is the marker that binds to (X). This test is very (sensitive/specific).

A

X = auto-Ab in patient serum

Sensitive;
Normal individuals can test positive for this, so not very specific

37
Q

Detection of (X) is more reliable and specific for autoimmune disease testing, compared to ANA test.

A

X = Ab to specific Ag (ex: dsDNA, RNP, topoisomerase)

38
Q

Detection of (X) Abs is diagnostic of SLE

A

X = anti-DNA and anti-Smith

39
Q

Anti-histamine Ab common (60%) in (X) disease, but even more common (90%) in (Y).

A 
X = SLE
Y = drug-induced SLE
40
Q

Anti-Ro/SSA and Anti-La/SSB are anti-(X) Ab that are associated with (Y) disease.

A 
X = RNP
Y = Sjogren's
41
Q

Anti-topoisomerase I Ab is commonly associated with (X).

A

X = systemic scleroderma

42
Q

Autoimmune disease characterized by dry eyes/mouth.

A

Sjogren’s

43
Q

Sjogren’s can occur secondary to (X) disease(s).

A

X = SLE, RA, scleroderma

44
Q

T/F: Sjogren’s is never a primary disease (occurs with no underlying disease).

A

False - “sicca” syndrome

45
Q

Sjogren’s pathology: what’s the mechanism of the disease?

A

Infiltration (CD4, with some B/plasma cells) and fibrosis of lacrimal/salivary glands

46
Q

Sjogren’s disease: patients with high titers of (X) tend have have extra-glandular disease.

A

X = anti-SSA (Ro) Ab

47
Q

75% of patients with (X) disease have Rheumatoid Factor in the absence of RA.

A

X = Sjogren’s

48
Q

T/F: There is a genetic association with HLA alleles in Sjogren’s.

A

True (HLA-B8, DR3, DRW52)

49
Q

Primary offender in Sjogren’s disease appears to be (X) Ab.

A

NOT an Ab… CD4 cells are primary offenders

50
Q

Sjogrens: lymphadenopathy can occur due to (X). These patients are at 40-fold increased risk for (Z).

A 
X = B cell (follicular) hyperplasia
Z = malignant lymphoma
51
Q

Autoimmune disease characterized by excessive fibrosis throughout the body.

A

Scleroderma

52
Q

Which organs are typically affected in Scleroderma? Star that which is mostly affected.

A
  1. Skin*
  2. Lungs
  3. Heart
  4. Muscle
  5. GI tract/kidneys
53
Q

The GI tract is affected in (X)% of scleroderma patients. List the changes that occur.

A

X = 90

  1. Collagenous fibrous replacement of muscularis (esp esophagus, BARRETT’S)
  2. Loss of villi in small intestine (malabsorption)
54
Q

Kidney involvement occurs in (X)% of scleroderma patients. What are the changes that occur?

A

X = 67

Mainly fibrosis of blood vessel walls (HT in 30%)

55
Q

Leading cause of death in scleroderma patients:

A

Pulm disease (HT, interstitial fibrosis)

56
Q

T/F: Large joints are usually spared in RA.

A

True

57
Q

About (X)% of RA patients have auto-Ab, Ig(A/G/M) to (FAB/Fc) portion of Rheumatoid Factor, Ig(A/G/M).

A

X = 80
IgM
Fc;
IgG

58
Q

Most of the extra-articular manifestations of RA are caused by:

A

Circulating immune complexes

59
Q

RA: synovial fluid will be infiltrated by…

A

CD4 cells, plasma cells, macrophages

60
Q

RA: eventually, (X) grows from synovial lining and extends over (Y) of the joint.

A 
X = pannus (fibrovascular mass)
Y = cartilaginous cap
61
Q

RA: pannus formation in joint will lead to (X).

A

X = joint cartilage erosion and eventual fusion of bones (ankylosis)

62
Q

Pathology: what would you expect to see in section of Rheumatoid nodule?

A

Fibrinoid necrosis of collagen, surrounded by inflammatory cells

Rheum (6 decks)

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