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Questions and Answers
What is the primary immunoglobulin involved in natural antibody-mediated reactions against RBC antigens?
What is the primary immunoglobulin involved in natural antibody-mediated reactions against RBC antigens?
Which autoimmune condition is characterized by IgG autoantibodies binding to acetylcholine receptors?
Which autoimmune condition is characterized by IgG autoantibodies binding to acetylcholine receptors?
What mechanism primarily causes hemolytic disease of the newborn?
What mechanism primarily causes hemolytic disease of the newborn?
What is the effect of IgG in autoimmune hemolytic anemia (AIHA)?
What is the effect of IgG in autoimmune hemolytic anemia (AIHA)?
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Which condition involves antibodies that stimulate rather than block receptor activity?
Which condition involves antibodies that stimulate rather than block receptor activity?
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What component primarily contributes to the activation of complement in Type II hypersensitivity?
What component primarily contributes to the activation of complement in Type II hypersensitivity?
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Which autoimmune condition specifically targets the basement membrane of the lungs and glomeruli?
Which autoimmune condition specifically targets the basement membrane of the lungs and glomeruli?
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What is the role of IgM in incompatible ABO blood transfusions?
What is the role of IgM in incompatible ABO blood transfusions?
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Study Notes
Antibody-Mediated Hypersensitivity (Type II)
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IgG and IgM bind to cell surfaces, triggering several effects:
- Complement activation
- Antibody opsonization
- Hormonal receptor binding
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Damage/Effects:
- Red blood cells
- Solid tissues
- Functional effects (sometimes a type V hypersensitivity)
Immune-Mediated Hemolysis (Red Blood Cells)
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ABO and Rh antigens:
- ABO: Oligosaccharides triggering IgM natural antibodies
- Rh: Protein triggering IgG antibodies
- I-system: Self-antigen implicated in autoimmune hemolytic anemia (AIHA)
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IgM antibodies:
- Effective complement activators (MAC), damaging red blood cells.
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IgG antibodies:
- Less effective complement activators than IgM.
- Opsonize red blood cell fragments for phagocytosis by macrophages.
Types of Immune-Mediated Hemolysis
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Alloimmune hemolysis:
- Hemolytic disease of the newborn
- Gradual destruction of fetal IgG-coated red blood cells (RBCs) by macrophages in the spleen/liver.
- Incompatible ABO blood transfusions
- Rapid (seconds) destruction by IgM natural antibodies, causing RBC aggregation and complement activation.
Anti-Red Blood Cell Antibodies
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IgM:
- Effective complement activators; cause rapid cell lysis.
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IgG:
- Less effective complement activators.
- Opsonize RBC fragments for phagocytosis.
Autoimmune Hemolysis
- Triggered by infections, drugs, or as part of autoimmune diseases (e.g., Systemic Lupus Erythematosus (SLE)).
- B-cell clonal expansion leading to autoantibodies (AIAs).
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AIHA:
- IgG autoantibodies (warm antibodies)
- IgM autoantibodies (cold antibodies) that are active below 37° Celsius.
Type II Autoimmune Hypersensitivity Against Solid Tissues
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Goodpasture's syndrome (GPS):
- IgG autoantibodies against the basement membrane of lungs and glomeruli.
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Pemphigus:
- IgG autoantibodies against intercellular cement protein (desmoglein) leading to blistering skin conditions.
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Myasthenia gravis:
- IgG autoantibodies against acetylcholine receptors in skeletal muscles causing muscle weakness.
Graves' Disease (Type V Hypersensitivity "Stimulatory")
- Most common cause of hyperthyroidism, often in young women with family history.
- Linked to HLA-DR3.
- Auto-antibodies (IgG) bind to TSH receptors, mimicking TSH hormone stimulation, leading to increased thyroxine secretion.
- Exophthalmos (protruding eyes): T-cell infiltration of the orbit due to an autoimmune reaction.
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Description
Explore the mechanisms and effects of antibody-mediated hypersensitivity, specifically Type II. This quiz covers IgG and IgM interactions, their roles in hemolysis, and the implications on red blood cells and tissues. Test your understanding of these crucial immunological concepts.
