La Cava Antonio
Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095-1670, USA.
Curr Med Chem. 2009;16(12):1482-8. doi: 10.2174/092986709787909659.
In systemic lupus erythematosus (SLE), the interaction between hyperactive T cells and B cells causes a dysregulated production of autoantibodies that can lead to tissue damage and impaired organ function. Studies on the modalities of communication between T and B cells have led to the design of new therapeutics for SLE, including autoantibody-derived peptide immunotherapies. Since many autoantibodies in SLE patients have amino acid sequences similar to those of murine antibodies, and at similar locations, the current directions are to employ strategies that have given promising results in mice in human clinical settings. This review describes the experimental evidence, rationale, and preclinical models of autoantibody-derived peptide immunotherapy in SLE, and how this information is translating into clinical studies in humans.
在系统性红斑狼疮(SLE)中,过度活跃的T细胞与B细胞之间的相互作用会导致自身抗体产生失调,进而引发组织损伤和器官功能受损。对T细胞与B细胞之间通讯方式的研究促成了针对SLE的新疗法的设计,包括源自自身抗体的肽免疫疗法。由于SLE患者的许多自身抗体具有与鼠抗体相似的氨基酸序列,且位置相近,目前的方向是采用在小鼠实验中已取得有前景结果的策略应用于人类临床。本综述描述了SLE中源自自身抗体的肽免疫疗法的实验证据、原理及临床前模型,以及这些信息如何转化为人类临床研究。