01a: Immunology Flashcards by Nuna H

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

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

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

IV;

Both CD4 and CD8

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

False - small complexes (large ones get cleared rapidly)

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

Immune rxn specific for self Ag
Not simply secondary rxn to tissue injury
Absence of well-defined cause of disease

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

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

Type II

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

III;

X = nuclear

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

II;

X = Insulin receptor (Ab inhibits insulin binding)

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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).

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

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

III;

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

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

CD4: cytokine-mediated inflammation
CD8: direct killing

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

X = thymus or marrow
Y  = periphery

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

X = M
Y = G

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

Location in thymus
Self-peptide presented on APC
T-cell with self-reactive T-cell receptor

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

Apoptosis

2. Become T-regs

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

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

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

Receptor editing

2. Apoptosis

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List the three mechanisms of peripheral tolerance.

Anergy
T-regs
Activation-induced cell death

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

Suppress APCs that present self-antigens

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List the molecules essential for development of T-regs.

IL-2 receptor

2. FoxP3 (TF)

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List the general mechanisms by which T-regs work.

Immunosuppressive cytokine secretion (IL-10, TGFb)

2. Competitively block co-stim molecule B7

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T-Lymphocyte activation requires which receptor interactions with APC?

Main signal: T-cell receptor with Ag-MHC

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

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Mechanisms of anergy (peripheral tolerance).

Weak/absent co-stim molecule on peripheral APC

2. Inhibitory co-stim molecules expressed on lymphocytes

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

True

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

Anergy (functionally inactivated)

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List the inhibitory co-stim molecules on T cells.

CTLA4, PD1

List some examples of Type IV HS autoimmune diseases.

1. Type I DM 2. MS 3. RA 4. Crohn's 5. Guillain-Barré syndrome

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

X = traumatic injury exposes them 1. Testes 2. Brain 3. Eye

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

True

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

``` X = HLA Y = negative selection ```

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

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

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

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

Autoimmune diseases: epitope spreading refers to...

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

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

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

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

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

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

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

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

X = auto-Ab in patient serum Sensitive; Normal individuals can test positive for this, so not very specific

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

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

Detection of (X) Abs is diagnostic of SLE

X = anti-DNA and anti-Smith

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

``` X = SLE Y = drug-induced SLE ```

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

``` X = RNP Y = Sjogren's ```

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

X = systemic scleroderma

Autoimmune disease characterized by dry eyes/mouth.

Sjogren's

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

X = SLE, RA, scleroderma

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

False - "sicca" syndrome

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

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

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

X = anti-SSA (Ro) Ab

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

X = Sjogren's

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

True (HLA-B8, DR3, DRW52)

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

NOT an Ab... CD4 cells are primary offenders

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

``` X = B cell (follicular) hyperplasia Z = malignant lymphoma ```

Autoimmune disease characterized by excessive fibrosis throughout the body.

Scleroderma

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

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

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

X = 90 1. Collagenous fibrous replacement of muscularis (esp esophagus, BARRETT'S) 2. Loss of villi in small intestine (malabsorption)

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

X = 67 Mainly fibrosis of blood vessel walls (HT in 30%)

Leading cause of death in scleroderma patients:

Pulm disease (HT, interstitial fibrosis)

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

True

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

X = 80 IgM Fc; IgG

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

Circulating immune complexes

RA: synovial fluid will be infiltrated by...

CD4 cells, plasma cells, macrophages

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

``` X = pannus (fibrovascular mass) Y = cartilaginous cap ```

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

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

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

Fibrinoid necrosis of collagen, surrounded by inflammatory cells

01a: Immunology Flashcards

(62 cards)