Folder Title: AgAbHype
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Transcript of Folder Title: AgAbHype
Types II and III: Antibody-Mediated
and Antigen-Antibody Complex-Mediated
Immediate Hypersensitivity Folder Title: AgAbHype
Updated: November 16, 2011
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Four Types of Hypersensitive (Allergic) Responses
Type II Immediate Hypersensitivity:Antibody-Mediated Cytotoxic Attack
on Host Cells Complement-Mediated or ADCC* - Mediated *ADCC = Antibody-dependent Cell-mediated Cytotoxicity
RhBaby
Baby with Hemolytic Disease of the New-Born (HDNB)
Auto-antibody to Acetyl Choline Receptor: Blockage of Acetyl-Choline Signalling in Myasthenia GravisFrom Roitt,
4th Ed.
Fig. 23.16
Myasthen
Complement-dependent attack on Ig-Fc labelled acetyl choline receptors and progressive damage to muscle cell end-plate and loss of acetyl-choline receptors.
In Myasthenia Gravis, communication between the neurons and muscle fibers is being disrupted by
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1. A bacterial toxin that inhibits acetyl choline binding2. A monoclonal antibody to acetyl choline receptor
that is being used therapeutically.3. A genetic abnormality that leads to the production
of abnormal acetyl choline receptors.4. An autoantibody that leads to autoimmune attack on
acetyl choline receptors5. An autoantibody that ties up acetyl choline.6. An enzyme that removes the acetyl group from
acetyl choline (acetyl cholinesterase)
(Fill in the blank Question)In Erythroblastosis Fetalis , why does the
auto-immune reaction happen to the Rh+ fetus only in Rh- Mothers?
"Frustrated Phagocytosis" as a
Damage Mechanism
in Types II and III Hypersensitivity
From Roitt,4th Ed., Fig. 23.4
Frustrat
Type III Immediate Hypersensitivity:Antigen-Antibody Complex Mediated
Attack on Host TissuesLocalized: Arthritis, NephritisSystemic: Serum SicknessComplement-Mediated:• Complement Activation - General Response to AgAb
Deposition• Complement Deficiency - Failure to Clear Autoimmune AgAb Complexes e.g. Systemic Lupus Erythrematosis (SLE)
HypSen3
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 AntigenRole of Complement• Keeps AgAb from precipitating in tissues• Marks AgAb for Removal by Reticuloendothelial System• Complement Deficiency leads to AgAb Accumulation
AgAbDump
Antigen-generation and Persistence in Type III Immediate Hypersensitivity
Persistent Infection• Leprosy• Malaria• Viral hepatitis• Dengue hemorrhagic fever• Staphylococcal Endocarditis• Streptococcal glomerulonephritis• MononucleosisAutoimmunity• Rheumatoid arthritis• Systemic Lupus ErythrematosisPersistent Exogenous Acquisition (Inhalation of Ag)• Extrinsic Allergic Alveolitis (e.g. Fungal antigens)
AgRemain
A.D.A.M. Medical Encyclopedia.Goodpasture syndromeAnti-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 failure along with lung disease.However, some forms of the disease involve just the lung or kidney, not both.Causes, incidence, and risk factorsGoodpasture 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.
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.
Which of the following can lead to Type-III Hypersensitivity: Immune-complex Disease? (Enter all correct responses. Set them up as a string of numbers (e.g. 123678) then press
enter when you have all of the correct numbers in the string
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1. Failure to resolve an inflammatory disease.2. Failure of an antibody to recognize and antigen3. Auto-immune response to a self-antigen.4. Severe chronic immunodeficiency.5. High dose persistent exposure to an
immunogen.6. Defect in complement response.7. Systemic treatment with a therapeutic
immunogen.8. Over-production of IgE antibody
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