作者: William Stohl
DOI: 10.1007/978-1-59259-703-1_18
关键词: Antigen 、 Graft-versus-host disease 、 Antigen specific 、 Autoantibody production 、 T cell 、 Cytolysis 、 Pathogenesis 、 Immunology 、 Immune system 、 Medicine
摘要: Considerable understanding of immune dysfunction in systemic lupus erythematosus (SLE) has been achieved. Nevertheless, the underlying etiopathogenesis SLE remained largely enigmatic. In both murine and human SLE, antigen- non—antigen-driven components each contribute to autoantibody production characteristic disorder (1,2). this chapter, which deals with impaired T-cell cytolytic activity its ramifications for pathogenesis, focus is on (polyspecific) component. This emphasis non—antigen-specific does not, any way, mitigate fundamental importance pathogenesis antigen-driven processes. Rather, by emphasizing a defect regulation responses, chapter aims reinforce central role that plays development clinical SLE.