浙江大学医学院：超敏反应（PPT讲稿）Hypersensitivity

Hypersensitivity(超敏反应) Jianzhong chen Institute of immunology Zhejiang University School of Medicine chenjianzhong@zju.edu.cn

Hypersensitivity (超敏反应) Jianzhong Chen Institute of Immunology Zhejiang University School Of Medicine chenjianzhong@zju.edu.cn

Type II hypersensitivity cytotoxic type) a Type Ii hypersensitivity reactions are mediated by igg and igm antibody binding to specific cells or tissues. The damage caused is thus restricted to the specific cells or tissues bearing the antigen. a The antibodies damage cells and tissues by activating complement and by binding and activating effector cells carrying FcyR

Type II hypersensitivity (cytotoxic type)  Type II hypersensitivity reactions are mediated by IgG and IgM antibody binding to specific cells or tissues. The damage caused is thus restricted to the specific cells or tissues bearing the antigen.  The antibodies damage cells and tissues by activating complement, and by binding and activating effector cells carrying FcR

I Pathogenic mechanisms Ags on the surface of target cells body→IgG,IgM 1. damage the target cell 1) activation of complement 2) opsonization: FcR, C3bR 3)ADcc: nk cells,Mφ 2 target cell dysfunction

I. Pathogenic mechanisms Ags on the surface of target cells ↓ body→IgG, IgM ↓ 1. damage the target cell 1) activation of complement 2) opsonization: FcR, C3bR 3) ADCC: NK cells, M 2. target cell dysfunction

细胞表面固有抗原或吸附于 细胞表面的抗原、半抗原 十 相应抗体(gG、lg 激活补体 调理吞噬 NK细胞、吞噬细胞刺激或阻断作用 溶解靶细胞 吞噬破坏靶细胞 ADCC作用 靶细胞损伤 靶细胞功能改变 Ⅱ型超敏反应的发生机制

Type ll Hypersensitivity classical pathway complement activation nK cell MAC Antibody dependent cell cytotoxicity C2-C9 FeRⅢ5 macrophage opsonization

NK cell opsonization

(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

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