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Grave’s Disease
Autoantibodies mimic the action of TSH, overstimulating the thyroid
Hashimoto’s thyroiditis
Autoantibodies and TH1 lymphocytes cause a delayed-type
Autoimmune Hemolytic Anemia
Autoantibodies to red cell antigens lead to complement-mediated cell lysis or clearance of antibody coated cells by macrophages.
Systemic Lupus Erythematosis
Systemic disease in which anti-nuclear antibodies form complexes with antigen, leading to complement activation and damage to blood vessels.
Insulin-Dependant Diabetes Mellitus
In a delayed-type hypersensitivity reaction, cytotoxic lymphocytes destroy betacells in the islets of Langerhans, leading to decreased insulin production.
Rheumatoid Arthritis
IgM autoantibody that reacts with the Fc portion of IgG. Complexes deposit in joints, leading to complement activation and chronic inflammation
Myasthenia gravis
Autoantibodies block the acetylcholine receptors in muscle. Antibodies activate complement, leading to lysis of muscle cells.
Multiple Sclerosis
Activated T lymphocytes cause inflammation, leading to myelin destruction.
Central tolerance is developed in the:
Thymus and bone marrow
Thymocytes that react strongly with self antigens are removed from the immune system via the process of:
Negative selection

In peripheral tolerance, the lymphocyte that releases cytokines in order to suppress autoimmune reactions is the:
Treg cell
Which subset of T lymphocytes is most frequently implicated in autoimmune reactions?
TH1
Autoimmunity develops through molecular mimicry when
Antibodies to a pathogen cross react with self antigen
Patients with autoimmune diseases involving antigen-antibody complexes have been successfully treated with
Plasmapheresis
What is needed for an antigen to build tolerance?
High dose of antigen subvaneous, oral no adjuvant present lack of co-stimulators young host small complex
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