Morawski Peter A, Bolland Silvia
Laboratory of Immunogenetics, National Institute of Allergic and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
Laboratory of Immunogenetics, National Institute of Allergic and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA.
Trends Immunol. 2017 May;38(5):373-382. doi: 10.1016/j.it.2017.02.001. Epub 2017 Mar 6.
Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by a breakdown of self-tolerance in B cells and the production of antibodies against nuclear self-antigens. Increasing evidence supports the notion that additional cellular contributors beyond B cells are important for lupus pathogenesis. In this review we consider recent advances regarding both the pathogenic and the regulatory role of lymphocytes in SLE beyond the production of IgG autoantibodies. We also discuss various inflammatory effector cell types involved in cytokine production, removal of self-antigens, and responses to autoreactive IgE antibodies. We aim to integrate these ideas to expand the current understanding of the cellular components that contribute to disease progression and ultimately help in the design of novel, targeted therapeutics.
系统性红斑狼疮(SLE)是一种自身免疫性疾病,其特征是B细胞的自身耐受性破坏以及产生针对核自身抗原的抗体。越来越多的证据支持这样一种观点,即除B细胞外的其他细胞成分对狼疮发病机制也很重要。在本综述中,我们考虑了淋巴细胞在SLE中除产生IgG自身抗体之外的致病和调节作用方面的最新进展。我们还讨论了参与细胞因子产生、自身抗原清除以及对自身反应性IgE抗体反应的各种炎性效应细胞类型。我们旨在整合这些观点,以扩展目前对促成疾病进展的细胞成分的理解,并最终有助于设计新型靶向治疗方法。