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(A Complement- and Fc receptor-mediated inflammation Neutrophil activation receptors Complement 5a, C3a) Neutrophi Effector enzyme reactive oxygen inflammation and mechanisms of intermediates tissue injury activation Ab-mediated B Opsonization and phagocytosis Opsonized Fc receptor Phagocytosed diseases Phagocyte C3b receptor Phagocytosis Complement activation In myasthenia gravis (C) Abnormal physiologic responses without cell/tissue injury the abs against ach Nerve Graves' Antibody against nding Acetylcholine receptor inhibit TSH receptor disease TSH Antibody to (ACh) receptor ACh receptor neuromuscular ( Thyroid ACh transmission and cause epithelial cell ceptor paralysis Thyroid homones Antibody stimulates Antibody inhibits binding receptor without hormone of neurotransmitter to receptor CElsevierAbbas&LichtmanBasicImmunologyUpdated2e-www.studentconsult.corEffector mechanisms of Ab -mediated diseases Graves’ disease In myasthenia gravis the Abs against Ach receptor inhibit neuromuscular transmission and cause paralysis
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