Shen H H, Winchester R J
Springer Semin Immunopathol. 1986;9(2-3):143-59. doi: 10.1007/BF02099019.
The etiology of systemic lupus erythematosus (SLE) is determined in part by genetic factors which influence susceptibility to the disease. These factors presumably have a major role in determining the clinical and laboratory manifestations of SLE. Certain newer observations which may pertain to an understanding of the genetic basis of SLE will be critically reviewed in this chapter. These observations are based on advances in the analysis of human SLE and the increased knowledge provided by various murine models of human autoimmune processes. However, the specific genes involved and the mechanisms by which they exert their effect are at present still unknown. Special attention will be given newer insights into the role of genes of the major histocompatibility complex (MHC) and their relationship to the genes encoding the T cell antigen receptor. The role of classic immunoglobulin genes as well as more complex mechanisms involving preferential maternal or paternal genetic effects are also discussed. The contribution of genes encoding complement and complement receptors toward the expression of the disease state are discussed in brief.
系统性红斑狼疮（SLE）的病因部分由影响疾病易感性的遗传因素决定。这些因素可能在决定SLE的临床和实验室表现方面起主要作用。本章将对某些可能与理解SLE遗传基础相关的最新观察结果进行批判性综述。这些观察结果基于人类SLE分析的进展以及各种人类自身免疫过程小鼠模型提供的更多知识。然而，目前仍不清楚具体涉及哪些基因以及它们发挥作用的机制。将特别关注对主要组织相容性复合体（MHC）基因的作用及其与编码T细胞抗原受体基因的关系的新见解。还将讨论经典免疫球蛋白基因的作用以及涉及母系或父系遗传效应偏好的更复杂机制。简要讨论了编码补体和补体受体的基因对疾病状态表达的贡献。
