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Links between type I interferons and the genetic basis of disease in mouse lupus.

机译：I型干扰素与小鼠狼疮疾病的遗传基础之间的联系。

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摘要

Systemic lupus erythematosus (SLE), like other autoimmune diseases, is a complex genetic trait with contributions from both major histocompatibility complex (MHC) genes and multiple non-MHC genes. Most of the contributing genes have yet to be identified. Studies of mouse models of lupus have provided important insight into the immunopathogenesis of lupus-like IgG autoantibody production and lupus nephritis, and genetic analyses of these mice are helping to unravel the complex and heterogeneous genetic basis of disease. Recent studies in both human SLE and mouse models of lupus have emphasized a potential role of type I interferons (IFN-alpha/beta) in the initiation and perpetuation of disease. There is now increasing interest in genes that affect IFN-alpha/beta expression-activity and IFN-regulated target genes that may be involved in the disease process. One example is interferon-inducible gene 202 (Ifi202), which has been identified as a major candidate susceptibility gene in the New Zealand hybrid model of lupus. Studies suggest that increased expression of this transcription factor leads to lupus through inhibition of lymphocyte apoptosis, although its effects on immune function are extremely complex and have yet to be fully defined. This review will focus on the genetic basis of disease in mouse lupus with a special emphasis on those genetic contributions that may affect IFN-alpha/beta activity and those that may be target genes of IFN-alpha/beta action.
机译：像其他自身免疫性疾病一样，系统性红斑狼疮（SLE）是一种复杂的遗传特征，主要组织相容性复合体（MHC）基因和多个非MHC基因均具有贡献。大多数贡献基因尚未确定。狼疮小鼠模型的研究为狼疮样IgG自身抗体的产生和狼疮肾炎的免疫发病机理提供了重要的见识，对这些小鼠的基因分析有助于阐明疾病的复杂且异质的遗传基础。在人类SLE和狼疮小鼠模型中的最新研究都强调了I型干扰素（IFN-α/β）在疾病的引发和永存中的潜在作用。现在人们对影响IFN-α/β表达活性的基因和可能参与疾病过程的IFN调控靶基因的兴趣日益增加。一个例子是干扰素诱导基因202（Ifi202），它已被确定为新西兰狼疮杂交模型的主要候选易感基因。研究表明，尽管这种转录因子对免疫功能的影响极为复杂，并且尚未完全阐明，但该表达因子的表达增加可通过抑制淋巴细胞凋亡而导致狼疮。这项审查将侧重于小鼠狼疮疾病的遗传基础，特别着重于那些可能影响IFN-α/β活性的遗传贡献以及那些可能是IFN-α/β作用的靶基因的遗传贡献。

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