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Immunology > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

Autoimmune diseases operate by what types of hypersensitivity?

A
  1. Type II - cytotoxic
  2. Type III - immune complex
  3. Type IV - T-cell mediated/delayed
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2
Q

What causes autoimmunity?

A
  • Developmental regulation disfunction
  • Genetics
  • Environment

NO ONE FACTOR CAN CAUSE AUTOIMMUNITY

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3
Q

Mutations in what gene(s) is the most common genetic determinant of autoimmunity?

A

HLA - MHCI and MHCII

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4
Q

11% of caucasian people have the HLA-A1-B8-DQ2-DR3 haplotype, which is more likely to _______

A

bind self-antigen, thus predisposing them to autoimmunity

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5
Q

What are the 3 “immune-privileged” sites of the human body?

A
  1. Corneas
  2. Brain
  3. Testes
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6
Q

What is the only autoimmune disease that is more common in men than women?

A

Ankylosing spondylitis

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7
Q

What is the normal function of the autoimmune regulator (AIRE) gene?

A

Production of self-antigen to aide in negative selection

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8
Q

What is autoimmune polyglandular disease (APD)?

A
  • Autoimmune response against many endocrine glands
    • hypoparathyroidism
    • adrenal failure
    • ovarian failure
    • type I diabetes
    • candidiasis
    • enamel hypoplasia
    • nail dystrophy
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9
Q

What are the mechanisms that contribute to central tolerance? (3)

A
  1. Negative selection of B cells in the bone marrow
  2. Expression of tissue-specific proteins in the thymus so that they participate in negative selection of T-cells (AIRE)
  3. Negative selection of T-cells in the thymus
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10
Q

What are the mechanisms that contribute to peripheral tolerance? (3)

A
  1. Exclusion of lymphocytes from immune-privileged sites
  2. Induction of anergy in autoreactive B and T cells that reach the peripheral circulation
  3. Suppression of autoimmune responses by regulatory T-cells
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11
Q

Mutation of the X-linked FoxP3 gene causes a rare immunodeficiency that principally affects boys, called _______

A

immune dysregulation, polyendocrineopathy, enteropathy, X-linked disease (IPEX)

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12
Q

Children with IPEX have normal levels of _____ cells and elevated levels of ______ cells

A
  • CD25 T-reg cells
  • TH17 cells
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13
Q

How does IPEX present clinically?

A
  • Enteritis → chronic diarrhea
  • Type 1 diabetes
  • Eczema
  • Failure to thrive
  • Do not survive past 1 y/o
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14
Q

_____ tolerance is negative selection during lymphocyte development, occurring in primary lymphoid organs

A

Central tolerance

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15
Q

_____ tolerance refers to anergy or suppression of auto-reactive cells; occurring in secondary lymphoid organs

A

Peripheral tolerance

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16
Q

True or false, peripheral tolerance only occurs after infection occurs.

A

True

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17
Q

What is the consequence of a T-cell failing to receive a co-stimulatory signal from B7 on APCs?

A

Anergy

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18
Q

Binding of pathogen to self-protein results in _____

A

pathogen creating a unique epitope for autoimmunity to occur

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19
Q

How can disruption of cell tissue or barrier result in autoimmunity?

A

Unregulated release of cellular contents (self-antigen) can activate nontolerized lymphocytes

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20
Q

What is molecular mimicry?

A

Pathogen antigen resembles host antigen, which triggers production of cross-reactive antibodies or T-cells

21
Q

How do superantigens elicit an autoimmune reaction?

A

Stabilization of the MHC-TCR complex without the need for a co-stimulatory signal, thus activating potential auto-reactive T-cells

22
Q

Describe the Bystander effect in regard to B and T cells.

A

Self-reactive B/T cells receive second signal for activation from nearby cells

23
Q

Grave’s disease is associated with mutations in what gene?

A

HLA-DR3

24
Q

Describe the mechanism of Grave’s disease

A

Auto-IgG are generated against TSH receptor, however these antibodies are agonistic so they cause activation of the receptor and cause chronic overproduction of T3 and T4

25
Q

What are the symptoms of Grave’s disease?

A
  • Hyperthyroid
    • heat intolerance
    • nervousness
    • irritability
    • weight loss
    • bulging eyes
    • enlarged thyroid
26
Q

Grave’s disease can be treated with drugs that inhibit uptake of _____

A

Iodine

27
Q

True or false. If someone with Grave’s disease was pregnant, they cannot transfer the disease to their child.

A

False. IgG cross the placenta so the newborn will suffer the disease until the IgG is cleared

28
Q

Describe the mechanism of myasthenia gravis

A

Auto-IgG against acetylcholine receptors are antagonistic and marks them for endocytosis and degradation

29
Q

Describe the clinical presentation of myasthenia gravis in its early and late stages

A
  • Early - drooping eyelids (ptosis); double vision (diplopia)
  • Late - weakening of chest muscles; impaired breathing
30
Q

How do pyridostigmine and azathioprine work to treat myasthenia gravis?

A

Inhibits the breakdown of acetylcholine

31
Q

What are the differences between warm antibody types and cold antibody types in autoimmune hemolytic anemia?

A
  • Warm - IgG against RhD
  • Cold - IgM against glycophorin (I antigen)
    • only produced in individuals that live in cold climates (advised to move)
32
Q

Infection by _______ produces a mimicry response by cross-reacting with the I antigen on hemoglobin.

A

Mycoplasma pneumonia

33
Q

Describe the mechanism by which Rheumatic fever is triggered.

A
  • IgG against Streptococcus pyogenes cross-reacts with heart myosin, joints, and kidneys
  • Occurs weeks after infection
34
Q

Describe the mechanism by which Goodpasture’s syndrome develops

A
  • Auto-IgG against Type IV collagen against the glomerulus basement membrane
  • Triggers complement cascade leading to inflammatory damage
35
Q

How does Goodpasture’s syndrome present clinically?

A
  • Glomerulonephritis
  • Pneumonitis (in smokers)
  • Pulmonary hemorrhage (in smokers)
36
Q

How is Goodpasture’s syndrome treated?

A

Plasma exchange

37
Q

Rheumatoid arthritis is associated with mutations in what gene?

A

HLA-DR4

38
Q

Describe the two possible mechanisms by which Rheumatoid arthritis develops.

A
  1. Deposition of immune complexes in the joints (rheumatoid factor)
  2. Abs directed against citrullinated epitopes of self-proteins (peptidyl arginine deaminases); citrulline is a non-human amino acid
39
Q

What exactly is rheumatoid factor?

A

Auto-IgG directed against the Fc region of other IgG

40
Q

How do adalimumab and rituximab treat rheumatoid arthritis?

A
  • Adalimumab - antibodies against TNF-α
  • Rituximab - antibodies against CD20
41
Q

In Systemic Lupus Erythematosus (SLE), how are antinuclear antibodies generated?

A
  • UV radiation induces apoptosis and alteration of DNA structure
  • CD4 T-cells specific for self nucleosomal antigens produced
42
Q

In SLE, where do immune complexes deposit? (4) Consequences?

A
  1. Kidneys → glomerulonephritis
  2. Joints → arthritis
  3. Blood vessels → vasculitis
  4. Skin → rash
43
Q

How is SLE treated?

A
  • NSAIDs
  • Immunosuppressants
  • Biologics
44
Q

______ is caused by a CD4 TH1 response against a variety of thyroid antigens, leading to an infiltration of lymphocytes that destroy normal architecture and impairs thyroid function

A

Hashimoto’s thyroiditis

45
Q

How does cell architecture change in Hashimoto’s thyroiditis?

A

Thyroid becomes organized like lymphatic tissue

46
Q

How is Hashimoto’s thyroiditis treated?

A

Replacement thyroid hormone therapy

47
Q

Mutations in ______ confer susceptibility to type I diabetes, whereas ____ confers resistance and overrides the former.

A
  • DR4
  • DQ6
48
Q

Infections by _____ can induce type I diabetes by cross-reacting with insulin, glutamate decarboxylase, or protein components of β-islet cells, mediated by CD8+ T-cells

A
  • Coxsackie (A&B) virus
  • Echovirus
49
Q

Describe the mechanism by which celiac disease develops

A
  • TH1 cells release inflammatory cytokines
  • Macrophages activated
  • More cytokines and ROS
  • Destruction of intestinal epithelial cells

Immunology (13 decks)

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