(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.cor
Effector mechanisms of Ab -mediated diseases Graves’ disease In myasthenia gravis the Abs against Ach receptor inhibit neuromuscular transmission and cause paralysis
II, Clinical disease 1 Transfusion reactions A型血输血 A型血输入B型血体内 B型血体内存在抗A抗体 抗原 抗体 反应 A型血抗原 血细胞溶解 补体
II. Clinical disease 1. Transfusion reactions A型血 A型血抗原 A型血输入B型血体内 B型血体内存在抗A抗体 补体 抗原 抗体 反应 输血 血细胞溶解
2. Hemolytic disease of the newborn Mainly occurs when an Rh- mother gives birth to an rht infant Prevention: the administration of anti-rh ab to an rh- mother within 72 hours of delivering an Rh+ infant will prevent sensitization and problems with subsequent pregnancies
2. Hemolytic disease of the newborn Mainly occurs when an Rh- mother gives birth to an Rh+ infant. Prevention: The administration of anti-Rh Ab to an Rh- mother within 72 hours of delivering an Rh+ infant will prevent sensitization and problems with subsequent pregnancies
first birth postpartum subsequent pregnancy RhD mother B anti-Rh RhD+ red cells anti-RhD lysis RhD+ fetus RhD+ fetus
Y Y Y