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KN-Immunology Block 2 > L17: Autoimmunity > Flashcards

L17: Autoimmunity Flashcards

1
Q

What is an antagonist?

A

antibody that binds to a a cell surface receptor, thereby preventing its function

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2
Q

What is an agonist?

A

antibody that binds to a cell surface receptor in a way that mimics the binding of the actual ligand to the receptor.

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3
Q

Is autoimmune disease more common in males or females?

A

females

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4
Q

Give an example of an IgE-mediated autoimmune disease.

A

Autoimmune diseases are NEVER mediated by IgE antibodies.

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5
Q

What is autoimmune hemolytic anemia?

A

IgG and IgM bind to the surface of erythrocytes and activate complement through the classical pathway and then forms the MAC.
Bound antibody and C3b mediate clearance of RBCs from circulation by phagocytes in the spleen
RBC depletion results in a condition called anemia.
Commonly diagnosed with direct Coomb’s hemagglutination test

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6
Q

What is neutropenia?

A

low neutrophil count in blood. can be result of autoimmune response against antigens on their surface. Killed by phagocytes since nucleated cells are not efficiently killed by complement activation.

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7
Q

How is autoimmune neutropenia commonly treated?

A

splenectomy to reduce reate of spleen blood cell destruction

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8
Q

What is Goodpasture’s syndrome?

A

antibodies specific for extracellular matrix. alpha-chain of type IV collagen in the basement membranes. Antibodies deposit along basement membranes of renal glomeruli and renal tubules, eliciting inflammatory responses. Results in impaired kidney function and failure.

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9
Q

How is Goodpasture’s syndrome treated?

A

plasma exchange to remove self-reactive ABs and immunosuppressive drug treatment to prevent production of new autoantibodies.

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10
Q

What is acute rheumatic fever?

A

antibodies are produced in response to bacterial infection cross-react with self antigens of the human heart and become autoantibodies. Because T cells do not recognize the strep surface antigens, so B cells are not fully activated and there is no immunological memory, making the disease transient. Symptoms of chest pain, fever, weakness, fatigue, and joint pain

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11
Q

What is Grave’s disease?

A

antibodies bind to thyroid stimulatory hormone receptor and actually mimic binding of TSH to the receptor, resulting in chronic overproduction of thyroid hormone which causes hyperthyroidism. Heat intolerance, nervousness, irritability, warm moist skin, weight loss, enlargment of the thyroid, bulging eyes and a characteristic stare. Autoimmune response is biased towards TH2 response since there is little-to-no tissue destruction. The THS receptor antibodies are capable of crossing the placenta and can afflict the child

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12
Q

How is Grave’s disease treated?

A

TSH-receptor specific antibodies can be removed via total exchange of blood plasma

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13
Q

What is Myasthenia gravis?

A

signal from nerve to muscle across the neuromuscular junction is impaired because of autoantibodies specific for acetylcholine receptors on muscle cells. Loss of muscle activation by neurons.

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14
Q

How is Myasthenia gravis treated?

A

immunosuppressive drugs to prevent autoantibody formation. Pyridostigmine inhibits cholinesterase, which degrades acetylchole and longer lived acetylcholine can better compete with the autoantiboides for binding.

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15
Q

What is Guillaain Barré syndrome? (GBS)

A

typically a result of molecular mimicry by campylobacter jejuni. IgG specific for gangliosides (components of human nerve tissues) cause an acute inflammatory demyelinating polyneuropathy (AIDP). Causes symetrical weakness in lower limbs, which rapidly ascends to the upper limbs and face. Difficulty swallowing and breathing, drooling and paralysis over the course of a few hours or days.

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16
Q

How is GBS treated?

A

plasma exchange and immunosuppressive drugs

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17
Q

What is Miller-Fisher syndrome?

A

a rare variant of GBS, where the paralysis develops in a descending fashion, initially affecting ocular muscles, then descending to arms.

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18
Q

What is Wegener’s Granulomatosis?

A

type II autoimmune diseases mediated by anti-neutorphil cytoplasmic antiboides or ANCAs (IgG), usually for proeinase-3. The ANCAs bind to neutrophils and activate them. The activated cells upregulate adhesin molecule expression and bind to vascular endothelial cells and degranulate, damaging the vasculature. Usually follows bacterial or viral infection (molecular mimicry). Symptoms of rhinitis, upper airway, eye and ear diseases, Airway distress, coin lesions in lungs, glomerulonephritis and renal failure, arthritis, skin purpura and nodules, and sensory neuropathy.
Rarely affects the heart, GI tract or brain.

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19
Q

What is type III autoimmune disease?

A

caused by immune complexes deposited in tissues

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20
Q

What is systemic lupus erythematosus (SLE)?

A

autoimmune disease caused by autoantibodies specific for many intracellular macromolecules present in all cells in the body (DNA, histones, ribosomes, etc). 90% have arthritis. affects tissues throughout the body. Is a progressive disease. Immune complexes are deposited in blood vesses, kidneys, joints and other tissues causing further inflammation. Many patients die of organ failure. mechanism not well known, but a single autoreactive CD4 T cell can lead to activation of B cells that are specific for many self-antigens.

21
Q

What is Type IV autoimmune disease?

A

T-cell mediated

22
Q

What is insulin-dependent diabetes mellitus? (IDDM)?

A

autoimmune disease that results in the selective destruction of insulin-producing cells in the pancreas. T-cell-mediated response activates CTLs that are specific for the Beta islet of Langerhans cells and they wipe it out. Usually affects children and if untreated can result in coma and death.

23
Q

How is IDDM treated?

A

daily injections of insulin

24
Q

What is rheumatoid arthritis?

A

autoimmune disease that results in chronic episodic inflammation of the joints. IgG, IgM and IgA which are specific for Fc regions of human IgG molecules are referred to as rheumatoid factor. Rheumatoid factor is usually present but not necessarily. Characteristic leukocyte infiltrate that includes CD4 and CD8 T cells, B cells, plasma cells, neutorphils and macros. TNF-alpha is one of the primary mediators of the tinflammation observed.

25
Q

How is rheumatoid arthritis treated?

A

physiotherapy and various anti-inflammatory and immunosuppressive drugs. TNF-alpha blockers are particularly effective.
AND
Rituximab, an antibody specific for B cell surface marker that causes ADCC and removal of B cells.

26
Q

What is multiple sclerosis?

A

autoimmune response directed at myelin sheath of nervous cells. Causes motor weakness, impaired vision, lack of coordination, spasticity. Can kill within a few years. Activated TH1 cells are main culprit. They produce IFN-gamma that activates macros in sclerotic plaques. The macros release proteases and cytokines which demyelinate.

27
Q

How is MS treated?

A

immunosuppressive drugs and IFN-B1 which reduces incidence of attacks.

28
Q

What is the animal model for MS?

A

experimental allergic encephalomyelitis.

29
Q

What s Sjogren’s syndrome?

A

a systemic T cell-mediated autoimmune disease that attacks exocrine glands that produce tears and saliva. Almost all are women. Usually dryness of mouth and eyes, skin, nose, vagina. Can also affect kidneys, vasculature, lungs, pancreas, PNS and brain. Diagnosed with blood tests for ANA antibody and rheumatoid factor, schirmer tests to measure tear production, salivary gland function, lip biopsy, and ultrasound of salivary glands.

30
Q

how is Sjogren’s syndrome treated?

A

no cure, but artificial tears and goggles can help with eyes. Anti inflammatories help a little.

31
Q

What is APECED? (aka APD, autoimmune polyglandular disease)

A

genetic absence of transcription factor AIRE, which normally induces expression of tissue-specific proteins in the thymus. Negative T cell selectino is impaired. Autoimmune B and T cell responses.

32
Q

What is sympathetic opthalmia?

A

if eye is ruptured by trauma, eye proteins can drain in to local lymph nodes, where they can be processed and presented to naive T cells. If an autoimmune response develops, killer T cells will destroy eye tissue

33
Q

What is rheumatic fever?

A

normal immune responsivenesss to a streptococcal pathogen, but the antibodies cross-react and become spefici for heart tissue.

34
Q

Where in the body can effector T cells go? What about naive T cells?

A

effector T cells can travel almost anywhere.

Naive T cells are restricted to blood and lymph tissue.

35
Q

What is autoimmune thrombocytopenic purpura?

A

IgG-mediated inhibition of an enzyme responsible for cleavage of von Wildebrand factor vWF, which links platelets and blood vessels with clots. Can also be caused by platelet-specific autoantibodies (IgG).
Symptoms: thrombocytopenia (low platelet count), bruising (purpura), neurological symptoms, microangioplastic hemolytic anemia. RBCs are damaged as they are pushed through microscopic clots.

36
Q

How is autoimmune thrombocytopenic purpura diagnosed?

A

observation of microangioplastic hemolytic anemia, low platelet counts, presence of schistocytes (broken RBCs).

37
Q

How is autoimmune thrombocytopenic purpura treated?

A

plasma transfusion. Rutiximab to kill B cells. RhoGam, steroids, splenectomy, infusion of gamma globulin

38
Q

What is schleroderma?

A

inflammatory destruction of vascular endothelial cells of arterioles and smooth muscles. Replacement with collagen and other fibrous materials. affects blood vessels, kidneys, liver, brain. Symptoms of localized or systemic skin thickening, hard, smooth , ivory colored areas of hardened skin. Rheumatoid factor not required for disease

39
Q

How is schleroderma diagnosed?

A

presence of anti-nuclear Abs, anti-topoisomerase Abs, and anti-centromere Abs (igGs)

40
Q

How is schleroderma treated?

A

no known cure or standard treatment. Try to use drugs that increase blood flow to extremities

41
Q

What is pemphigus vulgaris?

A

autoimmune condition mediated by IgG specific for 2 proteins (desmoglein 1 and 3); results in loss of cohesion in keratinocytes in the epidermis. Painful chronic blistering of the skin

42
Q

How is pemphigus vulgaris diagnosed?

A

punch biopsy of lesion followed by immunofluorescent staining (IgG4 Ab considered pathogenic)

43
Q

How is pemphigus vulgaris treated?

A

corticosteroids and other anti-inflammatory drugs, rituximax (CD20-specific mAb; B cell surface marker)

44
Q

Will a pregnant woman who suffers from Grave’s give birth to a child suffering from symptoms of autoimmune disease?

A

yes. IgG can cross the placenta and will remain with the child for several weeks

45
Q

Will a pregnant woman who suffers from Goodpasture’s give birth to a child suffering from symptoms of autoimmune disease?

A

yes. IgG can cross the placenta and will remain with the child for several weeks

46
Q

What is subacute bacterial endocarditis?

A

Type III IgG mediated inflammation of endocardium. Antibodies that bind to strep viridans and normal flora in damaged heart valves cause inflammation. Also mediated by phagocytes that recognize opsonized bacteria (IgG and complement opsonins); anaphylatoxins produced as part of the complement cascades also promote inflamamtion

47
Q

What is mixed essential cryoglobulinemia?

A

Type III malady characterized by production of cryoglobulins (Ig that become insoluble at reduced temperature. Sometime only light chains are produced (Bence Jones proteins). Usually there is a B cell proliferative disorder (multiple myeloma or Waldenstrom macroglobulinemia). Common after Hep C infection. Cryoglobulins bind to Fc regions of antibody molecules and cause immune complex dissorders. Symptoms of Meltzers triad (purpura, arthralgia, myalgia

48
Q

What is meltzer’s triad?

A

purpura, arthralgia and myalgia

KN-Immunology Block 2 (8 decks)

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