Fig. 5.14A ). These phagocytes express receptors for the Fc tails of IgG antibodies and for breakdown products of the C3 complement protein, and use these receptors to bind and ingest opsonized particles. Opsonized cells are usually eliminated in the spleen, and this is why splenectomy is of clinical benefit in some antibody-mediated diseases.
Antibody-mediated cell destruction and phagocytosis occur in the following clinical situations: (1) transfusion reactions, in which cells from an incompatible
Table 5.4 Examples of Antibody-Mediated Diseases (Type II Hypersensitivity)
Clinicopathologic Disease Target Antigen Mechanisms of Disease Manifestations
AutoimmunehemolyticanemiaRedbloodcellmembraneproteinsOpsonizationandphagocytosisofredHemolysis,anemiabloodcells
AutoimmunethrombocytopenicPlateletmembraneproteinsOpsonizationandphagocytosisofBleedingpurpura(Gpllb:Illaintegrin)platelets
GoodpasturesyndromeProteininbasementmembranesofComplement-andFcreceptor–Nephritis,lunghemorrhagekidneyglomeruliandlungalveolimediatedinflammation
AcuterheumaticfeverStreptococcalcellwallantigen;Inflammation,macrophageactivationMyocarditis,arthritisantibodycross-reactswithmyocardialantigen
MyastheniagravisAcetylcholinereceptorAntibodyinhibitsacetylcholinebinding,Muscleweakness,paralysisdown-modulatesreceptors http://ebooksmedicine.net enzymes, (C5a, C3a)
TSH receptor Antibody to Thyroid
Antibody inhibits binding of neurotransmitter to receptor
Fig. 5.14 Mechanisms of antibody-mediated injury. (A) Opsonization of cells by antibodies and complement components and ingestion by phagocytes. (B) Inflammation induced by antibody binding to Fc receptors of leukocytes and by complement breakdown products. (C) Anti-receptor antibodies disturb the normal function of receptors. In these examples, antibodies to the acetylcholine (ACh) receptor impair neuromuscular transmission in myasthenia gravis, and antibodies against the thyroid-stimulating hormone (TSH) receptor activate thyroid cells in Graves disease.
donor react with preformed antibody in the host (Chapter 12); (2) hemolytic disease of the newborn (erythroblastosis fetalis), in which IgG anti–red blood cell antibodies from the mother cross the placenta and cause destruction of fetal red blood cells (Chapter 7); (3) autoimmune hemolytic anemia, agranulocytosis, and thrombocytopenia, in which individuals produce antibodies to their own blood cells (Chapter 12); and (4) certain drug reactions, in which a drug attaches to plasma membrane proteins of red blood cells and antibodies are produced against the drug-protein complex.
• Inflammation. Antibodies bound to cellular or tissue antigens activate the complement system by the classical pathway (