Folder Title: AgAbHypeNoTP

1. Types II and III Immediate Hypersensitivity: Antibody-Mediated and Antigen-Antibody Complex-Mediated Folder Title: AgAbHypeNoTP Updated: November 02, 2012

2. Four Types of Hypersensitive (Allergic) Responses

3. Type II Immediate Hypersensitivity:Antibody-Mediated Cytotoxic Attackon Host Cells Complement-Mediated or ADCC* - Mediated *ADCC = Antibody-dependent Cell-mediated Cytotoxicity

8. Baby with Hemolytic Disease of the New-Born (HDNB) RhBaby

11. Auto-antibody to Acetyl Choline Receptor: Blockage of Acetyl-Choline Signalling in Myasthenia Gravis From Roitt, 4th Ed. Fig. 23.16 Myasthen

12. Complement-dependent attack on Ig-Fc labelled acetyl choline receptors and progressive damage to muscle cell end-plate and loss of acetyl-choline receptors.

13. (Fill in the blank Question)In Erythroblastosis Fetalis , why does the auto-immune reaction happen to the Rh+ fetus only in Rh- Mothers? Response Grid 0 of 94

14. "Frustrated Phagocytosis" as a Damage Mechanism in Types II and III Hypersensitivity From Roitt, 4th Ed., Fig. 23.4 Frustrat

15. Type III Immediate Hypersensitivity:Antigen-Antibody Complex MediatedAttack on Host Tissues Localized: Arthritis, Nephritis Systemic: Serum Sickness Complement-Mediated: • Complement Activation - General Response to AgAb Deposition • Complement Deficiency - Failure to Clear Autoimmune AgAb Complexes e.g. Systemic Lupus Erythrematosis (SLE) HypSen3

16. Features of AgAb-Complex Disposition Contributing to Type III Immediate Hypersensitivity: Normal Removal of AgAb Complexes • By macrophages (Ab binds to Fc receptor) • By RBC binding of C3b Opsin to CR1 (C3b-receptor); • Transport to Spleen for removal. Site of Accumulation of AgAb Complexes • At local sites (e.g. joints, kidneys, lungs) • Systemically - "Serum Sickness" Persistence of Triggering Antigen Role of Complement • Keeps AgAb from precipitating in tissues • Marks AgAb for Removal by Reticuloendothelial System • Complement Deficiency leads to AgAb Accumulation AgAbDump

17. Antigen-generation and Persistence in Type III Immediate Hypersensitivity Persistent Infection • Leprosy • Malaria • Viral hepatitis • Dengue hemorrhagic fever • Staphylococcal Endocarditis • Streptococcal glomerulonephritis • Mononucleosis Autoimmunity • Rheumatoid arthritis • Systemic Lupus Erythrematosis Persistent Exogenous Acquisition (Inhalation of Ag) • Extrinsic Allergic Alveolitis (e.g. Fungal antigens) AgRemain

18. Initial: Antigen-Antibody Complex Activation of Complement 1. Complement break-down product activation of Type 1 mast cell degranulation with histamine release. Extravasation of neutrophils. 2. Neutrophil activation by complement break-down products. Tissue damage by constant inflammation

21. Features of Rheumatoid Arthritis Auto-IgM-antibody attack (“Rheumatoid Factor” ) on the Fc region of IgG antibodies. Chronic antigen-antibody deposition in joint. Activation of complement and inducation of Type III hypersensitivity with chronic inflammation of joints. Effects also on cardiovascular, respiratory, and hematological systems. Elevated occurrence in women ages 40 to 60.

22. A.D.A.M. Medical Encyclopedia. Systemic lupus erythematosus Disseminated lupus erythematosus; SLE; Lupus; Lupus erythematosus; Discoid lupus Last reviewed: February 14, 2011. Systemic lupus erythematosus (SLE) is a long-term autoimmune disorder that may affect the skin, joints, kidneys, brain, and other organs. Causes, incidence, and risk factors Systemic lupus erythematosus (SLE) is an autoimmune disease, which means the body's immune system mistakenly attacks healthy tissue. This leads to long-term (chronic) inflammation. The underlying cause of autoimmune diseases is not fully known. SLE is much more common in women than men. It may occur at any age, but appears most often in people between the ages of 10 and 50. African Americans and Asians are affected more often than people from other races. SLE may also be caused by certain drugs. For information on this cause, see Drug-induced lupus erythematosus

23. A.D.A.M. Medical Encyclopedia. Goodpasture syndrome Anti-glomerular basement membrane antibody disease; Rapidly progressive glomerulonephritis with pulmonary hemorrhage; Pulmonary renal syndrome; Glomerulonephritis - pulmonary hemorrhage. Last reviewed: August 13, 2009. Goodpasture syndrome is a rare disease that can involve rapidly progressive kidney failurealong with lung disease. However, some forms of the disease involve just the lung or kidney, not both. Causes, incidence, and risk factors Goodpasture syndrome is an autoimmune disorder, a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue. Persons with this syndrome develop substances that attack a protein called collagen in the tiny air sacs in the lungs and the filtering units (glomureli) of the kidney. These substances are called anti-glomerular basement membrane antibodies. Glomerular basement membrane is a part of the kidneys that helps filter waste and extra fluid from the blood. Anti-glomerular basement membrane are antibodies against this membrane. They can lead to kidney damage. Sometimes the disorder is triggered by a viral respiratory infection or by breathing in hydrocarbon solvents. In such cases, the immune system may attack organs or tissues because it mistakes them for these viruses or foreign chemicals. The immune system's faulty response causes bleeding in the air sacs and inflammation in the kidney's filtering units. Men are eight times more likely to be affected than women. The disease most commonly occurs in early adulthood.

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