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首页> 外文期刊>International journal of clinical rheumatology. >Belimumab: the first US FDA approved biological therapy for systemic lupus erythematosus
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Belimumab: the first US FDA approved biological therapy for systemic lupus erythematosus

机译：Belimumab：首个美国FDA批准用于系统性红斑狼疮的生物疗法

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摘要

Systemic lupus erythematosus (SLE) is a complex multisystemic autoimmune disease with considerable clinical and immunological heterogeneity. Although the exact pathogenetic mechanisms have yet to be elucidated, both genetic and environmental factors are thought to be involved [1]. SLE is characterized by a myriad of immunological aberrations, which can be either the cause or effect of the disease. These abnormalities include aberrant apoptosis and defective clearance of apoptotic materials such as nuclear autoantigens and nucleosomes, as well as immune complexes by macrophages and the complement system [2], increased maturation of myeloid dendritic cells that drive the development of the proinflammatory Thl7 cells [3], and defective functions of the regulatory T cells (Tregs) leading to hyperactivity of the helper T cells and autoreactive B cells [4]. The end result is B-cell hyperactivity contributing to increased autoantibody production. Autoantibodies mediate tissue injury by the formation of immune complexes and subsequent complement activation, as well as through the direct mechanism of antibody-mediated cytotoxicity.
机译：系统性红斑狼疮（SLE）是一种复杂的多系统自身免疫性疾病，具有相当大的临床和免疫异质性。尽管尚未阐明确切的致病机制，但认为遗传和环境因素均涉及[1]。 SLE的特征是无数种免疫异常，可能是疾病的原因或结果。这些异常包括凋亡异常和凋亡物质如核自身抗原和核小体的清除缺陷，以及巨噬细胞和补体系统的免疫复合物[2]，髓样树突状细胞成熟的增加，从而促进促炎性Thl7细胞的发育[3]。 ]，以及调节性T细胞（Tregs）的功能缺陷，导致辅助性T细胞和自身反应性B细胞活动过度[4]。最终结果是B细胞过度活跃，导致自身抗体产生增加。自身抗体通过免疫复合物的形成和随后的补体激活以及抗体介导的细胞毒性的直接机制来介导组织损伤。

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