Immune Hypersensitivity Flashcards
Type I-III Hypersensitivites are antibody-mediated. How does Type IV Hypersensitivity differ?
Type IV is mediated by a direct T cell response
What cells and antibodies mediate Type I hypersensitivity?
Mast cells, IgE
Describe the process of priming in a type I hypersensitivity.
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.
Mast cells have a half-life of approximately 2-3 days. What is the influence of IgE on this half-life?
IgE can bind the FcRepisolon receptor on mast cells, increasing their half-life to approximately 3 weeks.
How does the immediate type I hypersensitivity response differ from that of the late-phase reaction?
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.
What are the pre-formed mediators of a type I hypersensitivity response?
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
What cytokines are released by Th2 cells to inhibit macrophage activation?
IL-4, IL-10
What is the function of IL-12 in a type I hypersensitivity response?
IL-12 is released by Th1 cells and inhibits a type I hypersensitivity response
Type II and III hypersensitivity responses are very similar. How do they differ?
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.
What are the three mechanisms of a Type II hypersensitivity?
Phagocytosis via opsonization
Inflammation
Antibody-mediated cellular dysfunction
What types of diseases are associated with type II Hypersensitivity?
Blood transfusion reactions, hemolytic diseases in newborns, autoimmune hemolytic disease, drug reactions
What is Rhogam?
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.
What disease is caused by anti-TSH receptor antibodies causing overproduction of T3 & T4?
Grave’s Disease - hypothyroidism
What disease is caused by the production of IgG antibodies that target and attack Type IV collagen in the kidney?
Goodpasture Syndrome
Type III hypersensitivity can cause systemic and localized reactions. What sites are favored for localized infections?
Kidneys, joints, skin, heart, small vessels
Tb skin tests and poison ivy reactions are what type of immune hypersensitivity?
Type IV - delayed hypersensitivity due to T cell activation
How does Type II Hypersensitivity response cause tissue damage and inflammation?
Complement and antibody are activated, recruiting neutrophils, enzymes, and ROS that stimulate inflammation and damage tissue.
What is Pemphigus vulgaris? What are the associated symptoms?
Autoantibody to desmosome cadherin results in the loss of cell-cell adhesion. This causes large blisters to form on skin and mucous membranes.
This disease is caused by an antibody to the Ach receptor, blocking Ach binding, and causing progressive muscle weakness.
Myasthenia Gravis
How does Systemic Lupus Erythematosus cause proteinuria? What type of hypersensitivity is this?
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.
How does Rheumatoid Arthritis damage joints?
IgG and IgM form immune complexes that collect in joints, causing damage. Some also infiltrate into synovial fluid.
