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Autoimmune Diseases Flashcards

1
Q

*Define autoimmunity

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2
Q

*Discuss possible mechanisms that may lead to autoimmune diseases

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3
Q

*Describe the factors that contribute to an individual’s risk for developing immune disease

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4
Q

*Define tolerance

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5
Q

*Explain why infection is often associated with the development of autoimmunity

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6
Q

*Identify the Specific target of each autoimmune disease and then describe the underlying pathogenic mechanism (type II, III, or IV hypersensitivity)

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7
Q

*Explain how epitope spreading impacts autoimmune responses and discusses underlying mechanism.

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8
Q

*Describe the specific clinical features associated with each disease and treatment options

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9
Q

What kind of hypersensitivity occurs with Poison ivy?

A

Poison Ivy- DELAYED hypersensitivity

Poison ivy - a type IV hypersensitivity

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10
Q

Describe a case study that occurs when one reacts to poison ivy

A

Case study-
7 year old develops itchy, red eruptions along his right arm 2 days following a hike in the woods
-over the course of the next 2 DAYS, the Rash spreads to his trunk face and genitals
-Diagnosed with DELAYED hypersensitivity to poison ivy
-prescribed: corticosteroid cream and oral Benadryl: patient does not improve
-Prescribe oral prednisone and lesions resolve approx 2 weeks.

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11
Q

What occurs during a TH1 cell mediated response? Differentiate between IFN-gamma and TFN-Beta

A

TH1 cell mediated- IFN-gamma- macrophage activation
TFN-Beta-
tissue destruction and macrophage activation
monocyte/macrophage chemotactic factor

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12
Q

No autoimmune diseases are mediated by which type of hypersensitivity?

A

NO AUTOIMMUNE Diseases are mediated by Type I Hypersensitivity or via Ig E.

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13
Q

Why is each subsequent reaction in a TH1 Cell mediated response more SEVERE?

A

Each subsequent reaction is more severe because every time you activate a cell, you make more Plasma/EFFECTOR cells and MEMORY CELLS, which makes response worse and worse

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14
Q

What clinical procedure would you use to confirm that patient’s hypersensitivity is caused by poison ivy?

A

To confirm hypersensitivity caused by Poison ivy, Apply PATCH containing poison ivy antigen (pentadecacatechol) to skin.
Since Poison ivy is Type IV hypersensitivity (form of contact dermatitis)
All Type IV Hypersensitivity- require PATCH TESTING
(look for erythemia and Induration after testing)

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15
Q

Compare and contrast the what procedures confirm patient’s hypersensitivity for type I vs Type IV?

A

Type I hypersensitivity- INJECTION of antigen intradermally

Type IV Hypersensitivity- use PATCH testing (apply patch to skin)

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16
Q

Describe the dependency for B cell and T cells

A

B cells are dependent on T cells

T cells do NOT depend on B cells

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17
Q

If a patient has X-linked agammaglobulinemia, what is the likelihood boy will develop poison ivy sensitivity upon exposure to plant?

A

X-linked agammaglobulinemia (NO B cells), the patient will have SAME likelihood as the general population to sensitivity upon exposure to this plant since they have no B cells, it will not impact antibodies?

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18
Q

Differentiate between type I, II, III hypersensitivity

A

Type I Hypersensitivity- IgE bind to receptor on Mast cells, basophils and have immediate response
Type II Hypersensitivity- antibody mediated immune reaction, where antibodies (like Ig G or Ig M) bind to cell surface antigens creating new epitope and inducing cellular lysis ( Cytotoxic cells)
ex: occurs in transfusion rxns, Hemolytic anemia, Rh factor; penicillin helps mediate this response
Type III Hypersensitivity- abnormal immune response due to excess of antigen (mouse antibody bind with antibody (soluble) on B cell), leading to formation of antibody-antigen aggregates called Immune complexes, This activates complement mech (CR1 and C3b) These complexes form precipitates. (antibody therapy used)
Type IV Hypersensitivity- Cell mediated immune reaction, interaction with T cells and antigen; T cells (TH1 CD4 cells) NO Antibodies.
Occurs in response to reaction to contact with certain allergens; CONTACT DERMATITIS, drug allergies.

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19
Q

Describe what occurs in Autoimmune diseases

A

Autoimmune diseases-

  • result from Adaptive immune responses against SELF antigens
  • Directed toward ELIMINATION of Normal/healthy components of the body
  • Leads to development of CHRONIC inflammation/disease and impair tissue/organ functions
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20
Q

What factors cause autoimmunity?

A

Causes of autoimmunity:

combination of genetic factors, Developmental factors (immune regulation) environment

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21
Q

Name the factors that affect susceptibility to Autoimmune diseases?

A

Factors that affect susceptibility to Autoimmune diseases:

  1. Genetics- HLA- MHC I and MHC II
  2. Race (white; 11% have HLA-A1-B8)
  3. Sex- (females have higher risk of developing disease
  4. Environmental (smoking, trauma, diet)
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22
Q

What is the #1 genetic determinant of Autoimmune diseases?

A

MHC I and MHC II are the No.1 genetic determinant of autoimmune disease.

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23
Q

Does MHC I or MHC II have have a greater risk of autoimmune disease? What alleles do MHC I or MHC II have?

A

Greater risk of autoimmune disease associated with MHC I.
ex: Ankylosing spondylitis (inflammation of joints) associated with MHC I
MHC I- have A, and BC alleles
MHC II- have DP, DQ, DR alleles

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24
Q

Do males or females have a higher risk of having an autoimmune disease and why? What autoimmune disease do males have a higher incidence in?

A

FEMALES have HIGHER risk of developing autoimmune disease than males
females- higher incidence (Addison’s disease, graves disease, rheumatoid arthritis, multiple sclerosis, Type 1 diabetes)
Males have higher incidence in Anklyosing spondylitis.
male and females (equal incidence in psoriasis, ulcerative colitis)

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25
Q

What are Immune privilege sites? Where are they located in body? what happens when there is trauma to these organs?

A

Immune privilege sites- places where immune system does NOT have access to.
ex: testes, brain and cornea
Trauma to these organs will cause antigens to come out and trigger an autoimmune condition.

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26
Q

When do autoimmune diseases arise?

A

Autoimmune diseases arise when Tolerance to self-antigens is LOST.

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27
Q

What are the mechanisms that contribute to immunological self-tolerance?

A

Mechanisms that lead to immuno self-tolerance:

  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
  3. Negative selection of T cells in Thymus
  4. Exclusion of lymphocytes from certain peripheral tissues: brain, eye and testes (Immune privilege site)
  5. Induction of anergy in autoreactive B and T cells that reach peripheral circulation
  6. Suppression of autoimmune responses by Regulatory T cells (T reggs express FOXp3)
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28
Q

What is the role of AIRE? What clinical condition occurs due to absence of AIRE?

A

AIRE- Autoimmune regulator protein- transcription factor that ensure negative selection is Complete (located in thymus) and involved in Central tolerance
Absence of AIRE leads to: (immune cell attacking body’s own organs)
Autoimmune Polyglandular Disease (APD) or Autoimmune polyendocrinopathy- cadidasis-ectodermal Dystrophy (APECED)
- which begins in INFANCY
-you have an immune response against many tissues including Endocrine glands
-Hypothyroidism, adrenal failure, ovarian failure, type I diabetes,
-Candidiasis (fungal infection of skin/mucous membranes due to yeast), dental enamel hypoplasia (thin enamel) and nail dystrophy (nails, rough thin and brittle)

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29
Q

What is role of FoxP3? What happens if there are mutations with FOXP3 expression?

A

FoxP3- transcription factor that controls T regg cells (CD4 T cells that suppress autoimmune responses)
Mutation in FoxP3- (you will not be able to suppress autoimmune cells)
leading to Immune Dysregulation, Polyendocrinopathy, enteropathy, and X-linked syndrome (IPEX)
- Have Normal levels of CD25 T-reg cells
-Elevated levels of TH17 cells
-Enteritis, Type 1 diabetes, Eczema
These diseases occur during Early childhood and may have symptoms of diarrhea. Children usually die within first year)

30
Q

What is tolerance? What occurs?

A

Tolerance- when a person does NOT respond to constituents of his/her body.
Lymphocytes that react against self-antigen are eliminated.

31
Q

Differentiate between central tolerance and Peripheral tolerance?

A

Central tolerance- negative selection during lymphocyte (B and T cell ) development; occurs in PRIMARY lymphoid organs
Peripheral tolerance- Anergy or Suppression; occurs in SECONDARY lymphoid organs.

32
Q

Further discuss Peripheral tolerance and the components involved.

A

In Peripheral Tolerance, you can have:
first signal: TCR (T-cell receptor ) react with Specific antigen (TCR react w/ MHC II on APC)
second signal: CD28 on T cell react with B7 Co-stimulator (co-stimulator only activated during sickness)
The interaction with TCR and antigen, co-stimulator will lead to T cell activation and proliferation
1. ANERGY: where you have specific antigen alone (NO co-stimulator) leading to T cell becoming ANERGIC
2. SUPPRESSION of Autoreactive T cells by regulatory T cells (Treggs). This suppression requires T reggs to interact with autoreactive T cells on the SAME Antigen presenting cells.
T reggs must interact with CD4 T cell on same APC.

33
Q

What are the first and second signals for T cell activation?

A

first signal: TCR (T-cell receptor ) react with Specific antigen (TCR react w/ MHC II on APC)
second signal: CD28 on T cell react with B7 Co-stimulator (co-stimulator only activated during sickness)
The interaction with TCR and antigen, co-stimulator will lead to T cell activation and proliferation

34
Q

Discuss the mechanisms of how Autoimmune diseases can be triggered by infection

A

How autoimmune diseases can be triggered by infection:
1. Disruption of tissue barrier: leading to release of sequestered self antigen; activation of nontolerized cells
ex: sympathetic opthalmia
2. Binding of pathogen to self-protein: pathogen acts to allow anti-self response (pathogen creates epitope that can be recognized as foreign) Ex: interstitial nephritis
3. Molecular mimicry- production of cross-reactive antibodies or T cells ex: Rheumatic fever, diabetes, multiple sclerosis)
4. Superantigen- polyclonal activation of autoreactive T cells
ex: rheumatoid arthritis. superantigen- nonspecific activation numerous T cells (no second signal needed)
5 Bystander effect: self-reactive B/T cells receive second signal for activation from cells nearby.

35
Q

What is the bystander effect?

A

Bystander effect: self-reactive B/T cells receive second signal for activation from cells nearby
- T cells specific for self-antigen, release signal
2. TCR and signal costimulator bind
When there is an absence of an infection: you do not receive signal 2, anergic.

36
Q

What occurs during a concurrent infection?

A

Concurrent infection:

37
Q

During T-cell activation, how can the requirement for 2nd signal be bypassed?

A

SUPERANTIGENS (Do not need 2nd signal)

38
Q

What factors are Antibodies directed against in type II hypersensitivity?

A

Antibodies (Ig M or Ig M) are directed against CELL SURFACE ANTIGENS
or Components of ECM.

39
Q

What autoimmune diseases are associated with Type II Hypersensitivity?

A

Type II Hypersensitivity: Antibodies (Ig M or Ig M) are directed against Cell Surface antigens or Components of ECM.

  1. Autoimmune Hemolytic Anemia-
  2. Goodpasture’s syndrome
  3. Acute rheumatic fever
  4. Grave’s disease
  5. Myasthenia gravis
40
Q

what is the autoantigen and consequence of autoimmune hemolytic anemia?

A

Autoimmune hemolytic anemia:
Autoantigen: Rh blood group antigens , I antigen
Consequence: Destruction of red blood cells, by COMPLEMENT and phagocytes, anemia.

41
Q

What is the autoantigen and consequence of Goodpasture’s disease?

A

Goodpasture’s Disease:
Autoantigen: Non-collagenous Domain of Basement membrane collagen type IV
Consequence: Glomerulonephritis, pulmonary hemorrhage

42
Q

What is the autoantigen and consequence of Acute rheumatic fever?

A

Acute Rheumatic fever:
Autoantigen: streptococcal cell wall antigens, antibodies cross-react with cardiac muscle
consequence: Arthritis, myocarditis, late scarring of heart valves

43
Q

What is the autoantigen and consequence of Grave’s disease?

A

Graves’s disease-
Autoantigen: thyroid stimulating hormone receptor
consequence: HYPOTHYROIDISM

44
Q

What is the autoantigen and consequence of Myasthenia Gravis?

A

Myasthenia Gravis
Autoantigen: Acetylcholine receptor
consequence: Progressive Weakness

45
Q

What autoimmune diseases are associated with type III Hypersensitivity?

A

Type III hypersensitivity: Formation of immune complexes that deposit in tissues (Activate complement; due to Ig G)

  1. Systemic Lupus Erythematosus
  2. Rheumatoid arthritis
46
Q

What is the autoantigen and consequence of Systemic Lupus Erythematosus ?

A

Systemic Lupus Erythematosus
Autoantigen: DNA, histones, ribosomes, snRNP, ScRNP
Consequence: Glomerulonephritis, vasculitis, arthritis

47
Q

What is the autoantigen and consequence of Rheumatoid arthritis?

A

Rheumatoid Arthritis:
Autoantigen: Unknown synovial joint antigen
Consequence: joint inflammation and destruction

48
Q

What are the autoimmune diseases associated with Type IV Hypersensitivity?

A

Type IV Hypersensitivity: T-cell mediated (Effector T cells)

  1. Type 1 Diabetes (insulin-dependent diabetes mellitus)
  2. Multiple Sclerosis
  3. Hashimotos,
  4. Hyperthroidism
  5. Celiac Disease
49
Q

What is the autoantigen and consequence of Type 1 diabetes?

A

Type 1 Diabetes (insulin-dependent diabetes mellitus)
Autoantigen: Pancreatic Beta cell antigen
Consequence: Beta cell destruction

50
Q

What is the autoantigen and consequence of Multiple sclerosis?

A

Multiple sclerosis:
Autoantigen: Myelin basic protein, proteolipid protein
Consequence: Brain degeneration, paralysis

51
Q

Which of the autoimmune diseases under Type II hypersensitivity are receptor mediated?

A

Receptor mediated:

  1. Graves’s disease
  2. Myasthenia gravis
52
Q

Explain what occurs in Grave Disease, in terms of normal functions of thyroid, vs disease mechanism. What are the clinical features of the disease? How can Graves Disease be treated?

A

Grave Disease- Thyroid (organ-specific disease)
-associated with HLA-DR3
Normal function:
-Thyroid synthesizes and stores Thyroglobulin
-Pituitary secretes TSH (thyroid stimulating hormone)
TSH binds to TSH receptor
-causes conversion of thyroglobulin into tri-iodothyronine (T3) and thyroxine (T4)
Disease mechanism:
-Autoantibodies (IgG) against TSH receptor
- these antibodies acts as Agonists (mimic TSH) which lead to chronic OVERPRODUCTION of T3/T4
Clinical features:
-HYPERTHYROID- heat intolerance, nervousness, irritability, weight loss, bulging eyes, ENLARGED thyroid (goiter)
-Treatment with drugs that INHBIT uptake of IODINE
(no iodine, no T3, T4).

53
Q

How can Grave’s disease be transferred from mother to child?

A

Grave’s disease can be transferred from mom to child:
because the Ig G antibody can CROSS the PLACENTA and infect the FETUS.
Process:
1.Mother with Grave’s disease can make anti-TSHR antibodies
2. During pregnancy, antibodies cross the placenta into the fetus
3. Newborn infant will also suffer from Grave’s disease
4. but Plasmapheresis can remove maternal anti-TSHR antibodies and cure the infant’s disease.

54
Q

What occurs in the disease Myasthenia gravis? Describe the normal function vs disease mechanism and include clinical features and treatment.

A

Myasthenia gravis:
Normal function of NMJ:
- Neuron impulse will innervate muscle tissue, allow Ach to be released
-Ach to bind to Ach Receptor, Na+ influx, and trigger muscle contraction.
Disease: Autoantibodies (IgG) against Acetylcholine Receptor
-Antagonists- that cause ENDOCYTOSIS and DEGRADATION (antibodies block Ach receptor, prevent Ach from binding)
- due to endocytosis of Ach receptors, Signaling across neuromuscular junction is IMPAIRED.
Clinical features: Progressive MUSCLE WEAKNESS
early- Drooping of eyelids, double vision
late- weakening of chest muscles that lead to impaired breathing
Treatment; PYRIDOSTIGMINE (muscle strengthener) AZATHIOPRINE (immunosuppressant)

55
Q

Which diseases form autoantibodies against cell surface receptors? Be sure to include their anitgen, antibody and target cell?

A

GRAVES’S Disease and Myasthenia Gravis have autoantibodies against cell surface receptors.
1.Graves’ disease
antigen: thyroid-stimulating hormone receptor
antibody- agonist
consequence- hyperthyroidisim
target cell- Thyroid epithelial cell

  1. Myasthenia Gravis-
    antigen: Acetylcholine receptor
    antibody- Antagonist
    consequence- progressive muscle weakness
    Target cell- muscle
56
Q

Describe what occurs in autoimmune hemolytic anemia and the mechanism.

A

Autoimmune hemolytic Anemia-
mechanism- Ig G and IgM form autoantibodies against RBC antigens
1. Opsonization
-Fc receptors (in spleen, that phagocytize and cause erythrocyte destruction)
-Complement receptors- (lead phagocytosis and erythrocyte destruction)
2. Complement -mediated lysis
This disease is infection associated- MIMICRY
-with mycoplasma pneumonia- cross reactivity with I antigen
Warm antibody type: Ig G against RhD
Cold antibody type: Ig M against Glycophorin (I antigen)
- this cold ab only see in cold environments

57
Q

describe the mechanism and issues associated with Rheumatic Fever.

A

Rheumatic fever:
Infection associated- Molecular MIMICRY
Mechanism:
form antibodies (IgG) against S. pyogenes which cross-react with myosin found in heart, joints and kidneys
This will lead to inflammation/damage of heart, joints and kidneys
Process:
1. Streptococcal cell wall can stimulate antibody response
2. Some antibodies cross-react with heart tissue, causing rheumatic fever.
This disease can result from inadequate treatment of strep throat or scarlet fever.
Prevention- ANTIBIOTICS

58
Q

Describe what occurs in the disease Goodpasture’s syndrome and clinical features and treatment

A

Goodpasture’s Syndrome:
Mechanism
-Form autoantibodies (IgG) directed against Type IV Collagen of glomerulus basement membrane which leads to Activation of Complement. and also Inflammatory damage.
Clinical presentation:
glomerulonephritis (impact kidney) pneumonitis, pulmonary hemorrhage (bleeding from lung)
you are synching the organ, causing damage to alveoli
Treatment: Plasma exchange (remove plasma that contains harmful antibodies and replace with healthy plasma)
This disease that is an environmental stressor disease

59
Q

What kind of autoimmune diseases have type III hypersensitivity?

A

Type III Hypersensitivity

  1. Rheumatoid Arthritis
  2. Systemic Lupus Erthematosus.
60
Q

What occurs during Rheumatoid arthritis? What is the mechanism and clinical features associated with them. How can it be treated?

A

Rheumatoid arthritis:
most common Rheumatic disease (autoimmune): 1-3% of US
- 3:1 female: male (more prevalent in women)
-HLA- DR4 association
Mechanism (type III):
1) Rheumatoid factor (80%): make IgG , IgM and Ig A against self- Ig G (Rh factor directed against Fc receptor.
-Deposition of immune complexes in joints, lead to INFLAMMATION
2) Antibodies directed against citrullinated epitopes of self-proteins (peptidyl deaminases; that deaminate Arg to make citrate
Clinical presentation: ARTHRITIS
- progressive: proteinases/collagenases can extend damage to cartilage, ligaments, tendons,bones
Treatment: Adalimumab leads to formation of anti-TNF a antibodies (block TNF, and reduce joint swelling/damage)
-Rituiximab - anti-CD20 anitbodies
These drugs help shut off large part of inflammation.

61
Q

describe what happens in the disease Lupus Erythematosus (SLE) and the clinical features, treatment associated with it.

A

Systemic Lupus Erythematosus (SLE);
- 9:1 female: male (higher incidence in women)
- 1 in 500 incidence in individuals of African or Asian descent
-UV radiation can induce apoptosis and may alter DNA structure so that it is viewed as foreign (CD4 T cells specific for self nucleosomal antigens)
Mechansism/clinical presentation:
1. Autoantibodies against constituents of the cytoplasm and nucleus (progressive)
-HLA-DR3 linkagel lead to ribonuclear proteins
-HLA-DR2- linkage- lead to DS DNA
These are anti nuclear antigens (ANA)
2. Immune complexes deposit in
-kidneys- glomerulonephritis
-Joints- arthritis
-Blood vessels- vasculitis
-Skin- rash (butterfly)
Treatment- NSAIDS, immunosuppressants, biologics

62
Q

compare and contrast the appearance of a normal nephron vs one with lupus nephritis

A 
Normal nephron- round structure, solid
disease nephron (Lupus Nephritis)-  thickening of membrane, influx of inflammatory cells in glomerulus cells (causing antibody-antigen complex to precipitate)
63
Q

How can an antibody response to self antigens change?

A

The antibody response to self antigens can Broaden and Strengthen by EPITOPE SPREADING

64
Q

What is Epitope spreading? Explain the process

A

Epitope spreading- the autoimmune response spreads, and expands beyond the single initiating epitope.
A SINGLE T cell can activate MANY B cells.
process:
1.CD4 T cells specific for one epitope of a macromolecular complex can provide help to B cells for other accessible epitopes of complex
2. A B cell that internalizes a macromolecular complex can present antigens to T cells specific for any of the proteins of complex

65
Q

What are the autoimmune diseases that have type IV hypersensitivity?

A

Autoimmune disease (TYPE IV Hypersensitivity; T-cell mediated):

  1. Hashimoto’s thyroiditis
  2. Type I diabetes
  3. Celiac disease
66
Q

Describe the mechanism and clinical presentation for Hashimoto’s thyroiditis

A

Hashimoto’s Thyroiditis (organ specific disease)
- Chronic thyroiditis (slowly developing inflammation of thyroid)
-leads to hypothyroidism (decreased amount of thyroid hormone)
-CD4 TH1 response (also antibodies )
-Infiltration of lymphocytes destroys normal architecture and function
Thyroid becomes organized like lymphatic tissue
-(lymphatic tissue ectopic; nodules in germinal center)
Clinical presentation: HYPOTHYROIDISM- fatigue, weakness, weight gain, sensitivity to cold
Treatment: Replacement therapy with thyroid hormones.

67
Q

Describe the mechanism, and clinical presentation for type 1 diabetes

A

Type 1 Diabetes (aka Juvenile diabetes)
Onset: 9-14 years of age
1 in 300 incidence in people of European descent
DR4 and several DQ alleles (DQ2, DQ8) confer susceptibility
DQ6 confers RESISTANCE (overrides dq2, dq8)
Infection association- Coxsackie (A and B ) Virus, echovirus
Mechanism:
-antibody and T-cell response against insulin, glutamate decarboxylase and other proteins of Beta-islet cells lead to destruction (these cells are destroyed)
CD8 T cells MEDIATE destruction
Clinical presentation: Insufficient INSULIN levels to control blood sugar levels.

68
Q

What is the mechanism and clinical features for celiac disease? Is it an autoimmune disease?

A

Celiac Disease: NOT AN AUTOIMMUNE DISEASE
Hypersensitivity to Dietary gluten; lead to selective destruction of intestinal epithelial cells.
Affects up to 20% of white people
DQ2 (80%), DQ8 association
Mechanism:
CD4+ T cells (TH1) release inflammatory cytokines, which causes Mac activation, causing inflammatory cytokines, reactive oxygen species, and leading to destruction

69
Q

Describe the process of how inflammatory effector T cells respond in celiac disease

A

Celiac disease process:

  1. Gluten is degraded in gut lumen to give resistant fragment
  2. gluten fragment enters tissue and is deaminated by transglutaminase (convert glutamine to glutamic acid)
  3. Naive CD4 T cell responds to deaminated peptides presented by HLA-DQ
  4. Inflammatory effector T cells cause villous atrophy
70
Q

Differentiate between the appearance of jejunum in normal person vs one with celiac disease

A

Normal jejunum (of small intestine) - long, tall, has villi
Celiac diseased jejunum- REDUCED Absorption capacity, due to influx of inflammatory cells, villi will be damaged
Villi- shrink or flattened (atrophy)

71
Q

Discuss the different types of hypersensitivities and Allergy, transplantation and autoimmunity associated with it.

A 
1. Type I Hypersensitivity:
Allergy- Peanut
No transplantation; NO AUTOIMMUNITY
2. Type II Hypersensitivity-
Allergy- Chronic urticaria
Transplantation- hyperacute rejection
Autoimmunity- autoimmune hemolytic anemia
3. Type III Hypersensitivity
Allergy- Serum Sickness
Transplantation- chronic rejection
Autommunity- Systemic Lupus erythematotus
4. Type IV Hypersensitivity
Allergy- Poison Ivy
Transplantation- Acute rejection
Autoimmunity- Type 1 diabetes
72
Q

If you have a case study, with a boy’s fingernails not properly formed (brittle, rough), normal levels of all T-cell subsets, and presence of antibodies against islet cells of pancreas (no clinical signs of diabetes), what is the cause of boy’s condition?

A

MUTATION IN AIRE
-since fingernails are rough, dry (sign of nail dystrophy)
nail dystrophy is a symptom of mutation in AIRE.

Immunology (11 decks)

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