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白细胞介素-1、白细胞介素-6 和辅助性 T 细胞 2 抑制的感染意义。

Infectious Implications of Interleukin-1, Interleukin-6, and T Helper Type 2 Inhibition.

机构信息

Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Division of Allergy/Immunology/Rheumatology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA.

出版信息

Infect Dis Clin North Am. 2020 Jun;34(2):211-234. doi: 10.1016/j.idc.2020.02.003. Epub 2020 Apr 23.

DOI:10.1016/j.idc.2020.02.003
PMID:32334983
Abstract

Targeting interleukins that drive innate inflammation has expanded treatments of autoinflammatory and autoimmune disorders. Interleukin (IL)-1 inhibition has proven useful for monogenic autoinflammatory syndromes, and IL-6 inhibition for autoimmune arthritides. Biological therapies impeding these pathways impair detection and containment of pathogens, particularly invasive bacteria, reflecting the importance of IL-1 and IL-6 in communicating danger throughout the immune system. Biologics targeting T helper type 2 inflammation are used to treat specific allergic, atopic, and eosinophilic diseases. They may impair protections against local herpesvirus reactivations while augmenting antiviral responses to respiratory viruses. Their risks with helminth exposures have yet to be defined.

摘要

针对驱动固有炎症的白细胞介素已扩展了自身炎症性和自身免疫性疾病的治疗方法。白细胞介素(IL)-1 抑制已被证明对单基因自身炎症综合征有效,而 IL-6 抑制对自身免疫性关节炎有效。阻碍这些途径的生物疗法会削弱对病原体(尤其是侵袭性细菌)的检测和控制,这反映了 IL-1 和 IL-6 在整个免疫系统中传递危险信号的重要性。针对 T 辅助细胞 2 型炎症的生物制剂用于治疗特定的过敏、特应性和嗜酸性疾病。它们可能会削弱对局部单纯疱疹病毒再激活的保护作用,同时增强对呼吸道病毒的抗病毒反应。它们与寄生虫暴露的风险尚未确定。

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