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了解自身免疫:机制、易患因素和细胞因子疗法。

Understanding Autoimmunity: Mechanisms, Predisposing Factors, and Cytokine Therapies.

机构信息

Department of Molecular Science and Technology, Ajou University, Suwon 16499, Republic of Korea.

S&K Therapeutics, Ajou University Campus Plaza 418, Worldcup-ro 199, Yeongtong-gu, Suwon 16502, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Jul 12;25(14):7666. doi: 10.3390/ijms25147666.

Abstract

Autoimmunity refers to an organism's immune response against its own healthy cells, tissues, or components, potentially leading to irreversible damage to vital organs. Central and peripheral tolerance mechanisms play crucial roles in preventing autoimmunity by eliminating self-reactive T and B cells. The disruption of immunological tolerance, characterized by the failure of these mechanisms, results in the aberrant activation of autoreactive lymphocytes that target self-tissues, culminating in the pathogenesis of autoimmune disorders. Genetic predispositions, environmental exposures, and immunoregulatory disturbances synergistically contribute to the susceptibility and initiation of autoimmune pathologies. Within the realm of immune therapies for autoimmune diseases, cytokine therapies have emerged as a specialized strategy, targeting cytokine-mediated regulatory pathways to rectify immunological imbalances. Proinflammatory cytokines are key players in inducing and propagating autoimmune inflammation, highlighting the potential of cytokine therapies in managing autoimmune conditions. This review discusses the etiology of autoimmune diseases, current therapeutic approaches, and prospects for future drug design.

摘要

自身免疫是指机体对自身健康细胞、组织或成分的免疫反应,可能导致重要器官的不可逆损伤。中枢和外周耐受机制通过消除自身反应性 T 和 B 细胞在防止自身免疫中发挥着关键作用。免疫耐受的破坏,表现为这些机制的失败,导致靶向自身组织的自身反应性淋巴细胞异常激活,最终导致自身免疫性疾病的发病机制。遗传易感性、环境暴露和免疫调节紊乱协同作用导致自身免疫性疾病的易感性和起始。在自身免疫性疾病的免疫治疗中,细胞因子治疗作为一种专门的策略出现,针对细胞因子介导的调节途径来纠正免疫失衡。促炎细胞因子是诱导和传播自身免疫炎症的关键因素,突出了细胞因子治疗在管理自身免疫疾病方面的潜力。本文讨论了自身免疫性疾病的病因、当前的治疗方法以及未来药物设计的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c30/11277571/11aae0e94ff6/ijms-25-07666-g001.jpg

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