Immune Hypersensitivity Flashcards

1
Q

Type I-III Hypersensitivites are antibody-mediated. How does Type IV Hypersensitivity differ?

A

Type IV is mediated by a direct T cell response

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2
Q

What cells and antibodies mediate Type I hypersensitivity?

A

Mast cells, IgE

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3
Q

Describe the process of priming in a type I hypersensitivity.

A

The allergen is presented to Th2 cells by APCs. Th2 cells secrete IL-4 which results in differentiation of Th0 cells to Th2 and antibody switching to IgE. IL-5 is also secreted to activate eosinophils and IL-13 to promote mucus secretion and airway remodeling.

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4
Q

Mast cells have a half-life of approximately 2-3 days. What is the influence of IgE on this half-life?

A

IgE can bind the FcRepisolon receptor on mast cells, increasing their half-life to approximately 3 weeks.

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5
Q

How does the immediate type I hypersensitivity response differ from that of the late-phase reaction?

A

The immediate response is often vasodilation, vascular leakage, and spasms due to histamine and other pre-formed compounds. Late-phase reactions include eosinophil infiltration, epithelial damage, and bronchospasm due to cytokines, prostaglandins, and leukotrienes.

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6
Q

What are the pre-formed mediators of a type I hypersensitivity response?

A

Histamine, heparin - anti coagulant, Chondroitin sulfate, enzymes- proteases hydrolases that cause production of kinins and C3a, TNF-alpha - stored in mast, activates endothelial, creates more adhesions, recruit, alter airways

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7
Q

What cytokines are released by Th2 cells to inhibit macrophage activation?

A

IL-4, IL-10

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8
Q

What is the function of IL-12 in a type I hypersensitivity response?

A

IL-12 is released by Th1 cells and inhibits a type I hypersensitivity response

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9
Q

Type II and III hypersensitivity responses are very similar. How do they differ?

A

Type II responses is a tissue-specific response with damage in that tissue. Type III responses are activated in the blood, with damage depending on where the immune complex deposits.

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10
Q

What are the three mechanisms of a Type II hypersensitivity?

A

Phagocytosis via opsonization
Inflammation
Antibody-mediated cellular dysfunction

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11
Q

What types of diseases are associated with type II Hypersensitivity?

A

Blood transfusion reactions, hemolytic diseases in newborns, autoimmune hemolytic disease, drug reactions

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12
Q

What is Rhogam?

A

Prophylaxis given to Rh- mothers before to prevent reactions with Rh+ fetal blood. The drug binds mother Rh antibodies to prevent opsonization of fetal RBCs.

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13
Q

What disease is caused by anti-TSH receptor antibodies causing overproduction of T3 & T4?

A

Grave’s Disease - hypothyroidism

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14
Q

What disease is caused by the production of IgG antibodies that target and attack Type IV collagen in the kidney?

A

Goodpasture Syndrome

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15
Q

Type III hypersensitivity can cause systemic and localized reactions. What sites are favored for localized infections?

A

Kidneys, joints, skin, heart, small vessels

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16
Q

Tb skin tests and poison ivy reactions are what type of immune hypersensitivity?

A

Type IV - delayed hypersensitivity due to T cell activation

17
Q

How does Type II Hypersensitivity response cause tissue damage and inflammation?

A

Complement and antibody are activated, recruiting neutrophils, enzymes, and ROS that stimulate inflammation and damage tissue.

18
Q

What is Pemphigus vulgaris? What are the associated symptoms?

A

Autoantibody to desmosome cadherin results in the loss of cell-cell adhesion. This causes large blisters to form on skin and mucous membranes.

19
Q

This disease is caused by an antibody to the Ach receptor, blocking Ach binding, and causing progressive muscle weakness.

A

Myasthenia Gravis

20
Q

How does Systemic Lupus Erythematosus cause proteinuria? What type of hypersensitivity is this?

A

Type III Hypersensitivity - Antibodies against DNA, histones, and ribosomes form immune complexes that deposit in the glomeruli, causing proteinuria. Systemic lupus can also cause rashes.

21
Q

How does Rheumatoid Arthritis damage joints?

A

IgG and IgM form immune complexes that collect in joints, causing damage. Some also infiltrate into synovial fluid.