Anticytokine autoantibodies are an emerging disease etiology, through the disturbance of physiological functions of cognate cytokines. Anti-interferon (IFN)-γ autoantibodies (AIGAs) were first identified in patients with severe mycobacterial infections, and were considered to be an autoimmune phenocopy of inborn genetic errors of the IL-12/IFN-γ axis. More than 600 reported cases, most originating from Southeast Asia, have been diagnosed over the last decade. Specific HLA class II molecules are associated with these autoantibodies, which provide a genetic basis for the high prevalence of this immunodeficiency syndrome in certain ethnic groups. Salmonellosis and herpes zoster reactivation are observed in more than half the patients with AIGAs. Moreover, AIGAs have been shown to underlie severe Taralomyce marneffei infection in HIV-negative patients. AIGAs may, thus, be considered a new form of late-onset immunodeficiency conferring a predisposition not only to severe mycobacterial, but also to some bacterial and fungal infections.

抗细胞因子自身抗体是一种新兴的疾病病因，通过同源细胞因子的生理功能的干扰。抗干扰素 (IFN)-γ 自身抗体 (AIGA) 首次在患有严重分枝杆菌感染的患者中发现，并被认为是 IL-12/IFN-γ 轴先天遗传错误的自身免疫表型。在过去十年中，已诊断出 600 多例报告病例，其中大部分来自东南亚。特定的 HLA II 类分子与这些自身抗体相关，这为这种免疫缺陷综合征在某些种族群体中的高流行提供了遗传基础。在超过一半的 AIGA 患者中观察到沙门氏菌病和带状疱疹再激活。此外，AIGA 已被证明是严重马尔尼菲酵母菌的基础HIV 阴性患者的感染。因此，AIGA 可能被认为是一种新形式的迟发性免疫缺陷，它不仅易患严重的分枝杆菌，而且易患某些细菌和真菌感染。