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Immunology > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

What two key features lead to autoimmunity?

A
  1. Failure of self-tolerance (self-reactive B or T cells)

2. Tissue destruction due to inflammation

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2
Q

What is the difference between autoimmunity and autoimmune disease?

A

autoreactive Ab or self-reactive T cells cause autoimmunity, but they will not cause disease unless there is inflammation (due to type II, III, or IV hypersensitivity)

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3
Q

What are the 5 major symptoms of inflammation?

A
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. loss of function
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4
Q

Are autoimmune diseases usually acute or progressive (chronic)?
What two things tend to cause acute/transient autoimmunity?

A

They are chronic and worsen with time, although there can be acute flares.

Acute/transient autoimmune disease is caused by drugs or infection

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5
Q

What is central tolerance?

A

Censoring of B or T cells in the primary lymphoid organs to make sure they are not self-reactive

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6
Q

What is peripheral tolerance?

A

censoring in secondary lymphoid organs

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7
Q

How does central tolerance of B cells work in the bone marrow?

A

B-cell editing - at the light chain locus
Anergy- if weakly reactive
Deletion- via apoptosis if strongly reactive

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8
Q

How does central tolerance of T cells work in the thymus?

A

High avidity–> deleted (negative selection)
No avidity–> deleted (neglect)
Low avidity–> survives and proliferates
AIRE presents tissue from the body that isn’t circulating through the thymus so T-cells will not be reactive to it

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9
Q

What are the three major ways peripheral tolerance are maintained?

A
  1. Sequester Ag
  2. Privileged sites
  3. regulatory cells (Treg, TGFb, IL-10)
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10
Q

What are 4 ways that antigens can be sequestered in the periphery to maintain tolerance?

A
  1. potentially autoreactive T and B may not gain access to the autoantigen tissue because it is not inflamed (lack addressins)
  2. There may not be MHC II molecules on the autoantigen tissue
  3. Most cells in the body lack CD80/86 which give signal 2 to the T-cell
  4. B-cells unactivated by Tcell CD40L undergo apoptosis via FAS/FASL
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11
Q

What are “immune privileged” sites of the body?

A

eyes, brain, uterus, testes

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12
Q

What are 3 ways that the body ensures B and T cells are not activated in immune privileged sites?

A
  1. physical barrier- BBB to block entrance of B and T
  2. Suppressive cytokines (IL-10, TGF-B)
  3. FASL expression on privileged sites to initiate apoptosis if B or T cells breach the physical barrier/get past suppressive cytokines
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13
Q

What cells in the body regulate autoreactivity of T and B cells? What TF activates these cells? What cytokines does it produce?

A

CD25, FOXP3 derived Treg cells supress the immune system by secreting IL-10 and TGF-B

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14
Q

Patients with mutations in AIRE develop what disorder?

A

APECED (APS1) where there is autoimmunity in endocrine glands due to the failure of self-antigens to be presented in the thymus

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15
Q

Patients with mutations in FAS/FASL develop what disorder?

A

ALPS- autoimmune lymphoproliferative syndrome because there is an accumulation of B and T cells that fail to be deleted (by fas)

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16
Q

What molecule downstream of fas can also cause ALPS?

A

caspases

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17
Q

Patients with defects in FOXP3 develop what disorder?

A

IPEX- because of defects in Treg function

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18
Q

Why does trauma increase the chance of an autoimmune response?

A

It breaches physical barriers and releases sequestered or privileged site antigens

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19
Q

What are the 4 ways infections can increase the chance for autoimmune disease?

A
  1. infection upregulates MHCII, CD80/86 to activate T and B cells
  2. engage TLR to activate innate immune system
  3. damage barriers- release privileged Ag
  4. Molecular mimicry
20
Q

What is molecular mimicry?

A

B or T cells recognize epitopes on pathogens that are very similar to host epitopes. Activated pathogens thus kill the pathogens, but also kill self proteins

21
Q

What self protein do streptococcus A proteins resemble? What does this cause?

A

cardiac myosin–> rheumatic heart disease

22
Q

What self proteins do campylobacter jejuni proteins resemble? What problem does this cause?

A

Myelin gangliosides and glycolipids on neurons–> Guilain Barre Syndrome (neural disease)

23
Q

What is sympathetic opthalmia?

A

Trauma to the left eye cause inflammation in the right eye 3 weeks later because there is a release of intraocular protein to the other eye

24
Q

What are 4 examples of breach of a physical barrier causing autoimmunity?

A
  1. sympathetic opthalmia
  2. vasectomy (broken barrier allows anti-sperm Ab to be released–> infertility)
  3. lens surgery
  4. smoking–>Goodpasture’s disease in lungs/kidneys
25
Q

How do drugs trigger autoimmunity?

A
  1. drugs generate neoepitopes out of self-antigens that trigger B and T cells for the new epitopes.
    (Penicillamine and m-DOPA)
  2. Bind to RBC and act as haptens–> autoimmune hemolytic anemia
26
Q

What are the four disorders associated with autoimmunity due to Type II hypersensitivity?

A
  1. Graves- overactive TSH-R
  2. Myasthenia Gravis- blocked AchR
  3. Goodpasture’s Disease- anti-NC1 domain of type IV collagen
  4. Autoimmune hemolytic anemia (AIHA)
27
Q

What is the autoantigen for AIHA?

What is the consequence?

A

Autoantigen against:
Factor I–> complement-mediated lysis of RBC
Rh+–> opsonization and destruction of RBC by phagocytes

28
Q

What is the autoantigen for Goodpasture’s syndrome?
What is the consequence?
What is a major cause?

A

Ab against the NC1 domain of type IV collagen in lungs and kidney–> glomerulonephritis and pulmonary hemorrhage

Often caused by smoking

29
Q

What is the autoantigen for Grave’s Disease?

What is the consequence?

A

Antagonistic reaction of TSH-R (thyroid stimulating hormone receptor)–> hyperthyroidism

30
Q

What is the autoantigen for Myasthenia gravis?

What is the consequence?

A

Anti-AchR which leads to progressive muscle weakness because less AP can be transferred at the neuromuscular junction

31
Q

What are the two types of Ab for autoimmune hemolytic anemia?
What is each directed against?

A
  1. Warm agglutinins- IgG directed against Rh+ antigen on RBC

2. Cold agglutinins- IgM to the I antigen on RBC

32
Q

How do warm agglutinins cause hemolytic anemia?

A

warm = IgG against Rh+ which coat the RBC with Ab and clear them by opsonization by splenic macrophages

33
Q

How do cold agglutinins cause hemolytic anemia?

A

IgM Ab lead to complement-mediated lysis of RBC by binding to I antigen–> Hb in the urine increases

34
Q

What clinical sign would let you know that the patient had hemolytic anemia due to cold agglutinins?

A

Increased Hb in the urine

35
Q

What is meant by transient autoimmunity?

A

When the mother’s IgG crosses the placenta, it can cause autoimmunity in the baby including:

  1. myasthenia gravis
  2. lupus
  3. hemolytic anemia
  4. graves
36
Q

What Ab are involved in neonatal lupus?

What is the clinical presentation?

A

anti-Ro and anti-La cause congenital heart block

37
Q

When do neonatal autoimmune diseases usually subside?

A

3-6 months because the mothers autoimmune IgG will nadir

38
Q

What are examples of autoimmune disorders with type 3 hypersensitivity?

A
  1. Rheumatoid arthritis

2. SLE (lupus)

39
Q

What is the autoantigen in rheumatoid arthritis?

What is the consequence?

A

Rheumatoid factor (IgM antiFC) –> immune complexes gather in joints

40
Q

What is the autoantigen in SLE?

What is the consequence?

A

Ab against chromatin, DNA and ribonucleoproteins –> immune-complex mediated glomerulonephritis, vasculitis, arthritis

41
Q

What type of immune complex is NOT pathogenic? Why?

A

large immune complexes because they are easily bound to FcR and complement and can be cleared

42
Q

What type of immune complex is not easily cleared from the body and gets deposited where circulation is sluggish? (what are these sites)

A

small immune complexes get deposited in:

  1. kidney
  2. Joints
  3. choroid plexus
  4. ciliary bodies
43
Q

What causes the autoimmune response when small ICs get deposited in sluggish circulation areas?

A

Fc and C3b are unable to be phagocytosed because they are stuck in the vascular wall.
Frustrated neutrophils release toxic mediators

44
Q

What are examples of autoimmunity with type IV hypersensitivity?

A

T1D, Hashimoto’s thyroiditis, RA, MS

45
Q

What cell is targeted by CTL in an autoimmune fashion in T1D? What is the consequence?

A

Pancreatic B cells leading to B-cell destruction and lack of insulin

46
Q

What is the autoantigen for Hashimoto’s thyroiditis? What is the consequence?

A

Thyroglobulin and thyroid peroxidase–> hypothyroidism and goiters

Immunology (25 decks)

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