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Autoimmune Diseases Flashcards

1
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*Define autoimmunity

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2
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*Discuss possible mechanisms that may lead to autoimmune diseases

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3
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*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
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*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
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*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?

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Poison Ivy- DELAYED hypersensitivity

Poison ivy - a type IV hypersensitivity

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10
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Describe a case study that occurs when one reacts to poison ivy

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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

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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?

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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?

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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?

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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?

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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

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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?

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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
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Differentiate between type I, II, III hypersensitivity

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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

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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?

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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?

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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?

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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?

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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?

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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
What are Immune privilege sites? Where are they located in body? what happens when there is trauma to these organs?
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.
26
When do autoimmune diseases arise?
Autoimmune diseases arise when Tolerance to self-antigens is LOST.
27
What are the mechanisms that contribute to immunological self-tolerance?
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)
28
What is the role of AIRE? What clinical condition occurs due to absence of AIRE?
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)
29
What is role of FoxP3? What happens if there are mutations with FOXP3 expression?
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
What is tolerance? What occurs?
Tolerance- when a person does NOT respond to constituents of his/her body. Lymphocytes that react against self-antigen are eliminated.
31
Differentiate between central tolerance and Peripheral tolerance?
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
Further discuss Peripheral tolerance and the components involved.
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
What are the first and second signals for T cell activation?
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
Discuss the mechanisms of how Autoimmune diseases can be triggered by infection
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
What is the bystander effect?
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
What occurs during a concurrent infection?
Concurrent infection:
37
During T-cell activation, how can the requirement for 2nd signal be bypassed?
SUPERANTIGENS (Do not need 2nd signal)
38
What factors are Antibodies directed against in type II hypersensitivity?
Antibodies (Ig M or Ig M) are directed against CELL SURFACE ANTIGENS or Components of ECM.
39
What autoimmune diseases are associated with Type II Hypersensitivity?
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
what is the autoantigen and consequence of autoimmune hemolytic anemia?
Autoimmune hemolytic anemia: Autoantigen: Rh blood group antigens , I antigen Consequence: Destruction of red blood cells, by COMPLEMENT and phagocytes, anemia.
41
What is the autoantigen and consequence of Goodpasture's disease?
Goodpasture's Disease: Autoantigen: Non-collagenous Domain of Basement membrane collagen type IV Consequence: Glomerulonephritis, pulmonary hemorrhage
42
What is the autoantigen and consequence of Acute rheumatic fever?
Acute Rheumatic fever: Autoantigen: streptococcal cell wall antigens, antibodies cross-react with cardiac muscle consequence: Arthritis, myocarditis, late scarring of heart valves
43
What is the autoantigen and consequence of Grave's disease?
Graves's disease- Autoantigen: thyroid stimulating hormone receptor consequence: HYPOTHYROIDISM
44
What is the autoantigen and consequence of Myasthenia Gravis?
Myasthenia Gravis Autoantigen: Acetylcholine receptor consequence: Progressive Weakness
45
What autoimmune diseases are associated with type III Hypersensitivity?
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
What is the autoantigen and consequence of Systemic Lupus Erythematosus ?
Systemic Lupus Erythematosus Autoantigen: DNA, histones, ribosomes, snRNP, ScRNP Consequence: Glomerulonephritis, vasculitis, arthritis
47
What is the autoantigen and consequence of Rheumatoid arthritis?
Rheumatoid Arthritis: Autoantigen: Unknown synovial joint antigen Consequence: joint inflammation and destruction
48
What are the autoimmune diseases associated with Type IV Hypersensitivity?
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
What is the autoantigen and consequence of Type 1 diabetes?
Type 1 Diabetes (insulin-dependent diabetes mellitus) Autoantigen: Pancreatic Beta cell antigen Consequence: Beta cell destruction
50
What is the autoantigen and consequence of Multiple sclerosis?
Multiple sclerosis: Autoantigen: Myelin basic protein, proteolipid protein Consequence: Brain degeneration, paralysis
51
Which of the autoimmune diseases under Type II hypersensitivity are receptor mediated?
Receptor mediated: 1. Graves's disease 2. Myasthenia gravis
52
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?
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
How can Grave's disease be transferred from mother to child?
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
What occurs in the disease Myasthenia gravis? Describe the normal function vs disease mechanism and include clinical features and treatment.
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
Which diseases form autoantibodies against cell surface receptors? Be sure to include their anitgen, antibody and target cell?
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 2. Myasthenia Gravis- antigen: Acetylcholine receptor antibody- Antagonist consequence- progressive muscle weakness Target cell- muscle
56
Describe what occurs in autoimmune hemolytic anemia and the mechanism.
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
describe the mechanism and issues associated with Rheumatic Fever.
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
Describe what occurs in the disease Goodpasture's syndrome and clinical features and treatment
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
What kind of autoimmune diseases have type III hypersensitivity?
Type III Hypersensitivity 1. Rheumatoid Arthritis 2. Systemic Lupus Erthematosus.
60
What occurs during Rheumatoid arthritis? What is the mechanism and clinical features associated with them. How can it be treated?
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
describe what happens in the disease Lupus Erythematosus (SLE) and the clinical features, treatment associated with it.
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
compare and contrast the appearance of a normal nephron vs one with lupus nephritis
``` 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
How can an antibody response to self antigens change?
The antibody response to self antigens can Broaden and Strengthen by EPITOPE SPREADING
64
What is Epitope spreading? Explain the process
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
What are the autoimmune diseases that have type IV hypersensitivity?
Autoimmune disease (TYPE IV Hypersensitivity; T-cell mediated): 1. Hashimoto's thyroiditis 2. Type I diabetes 4. Celiac disease
66
Describe the mechanism and clinical presentation for Hashimoto's thyroiditis
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
Describe the mechanism, and clinical presentation for type 1 diabetes
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
What is the mechanism and clinical features for celiac disease? Is it an autoimmune disease?
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
Describe the process of how inflammatory effector T cells respond in celiac disease
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
Differentiate between the appearance of jejunum in normal person vs one with celiac disease
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
Discuss the different types of hypersensitivities and Allergy, transplantation and autoimmunity associated with it.
``` 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
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?
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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