干扰素γ是一种抗菌信号蛋白质。科学家们发现一种分子，它能在干扰素γ大量出现时保护激活的免疫细胞，让它们得以生存。 他们在新出版的《自然—免疫学》期刊中报告说，在慢性感染出现时免疫能持续作出反应，Irgm1分子发挥了关键作用。慢性免疫反应出现在许多种类的寄生虫疾病中。
干扰素是一种抗菌化合物，有助于病毒和其他细胞病原菌的根除。但高浓度的干扰素对附近的细胞却是有毒的。因此，这是一个困境：制造干扰素应对感染的免疫细胞在这一过程中如何保全自己？
Carl Feng和同事鉴别出一种名为Irgm1 的分子，它在保护生产干扰素的免疫细胞免遭其毒素中毒的过程中发挥了关键作用。他们指出，面对干扰素γ时，缺失 Irgm1的小鼠免疫细胞无法增生，并进入一种名为凋亡的细胞自杀过程。免疫细胞的减少导致感染的失控，所有的小鼠在被感染后都死了。然而，既缺乏 Irgm1又缺乏干扰素γ的小鼠却存活下来了，表明Irgm1保护了这些免疫细胞不受干扰素γ毒性的影响。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology，9, 1279 - 1287，Carl G Feng，Alan Sher
The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-γ-induced cell death
Carl G Feng1,6, Lixin Zheng2,6, Dragana Jankovic1, André Báfica1, Jennifer L Cannons3, Wendy T Watford4, Damien Chaussabel5, Sara Hieny1, Patricia Caspar1, Pamela L Schwartzberg3, Michael J Lenardo2 & Alan Sher1
Abstract
Mice deficient in the interferon-γ (IFN-γ)-inducible, immunity-related GTPase Irgm1 have defective host resistance to a variety of intracellular pathogens. This greater susceptibility to infection is associated with impaired IFN--dependent macrophage microbicidal activity in vitro. Here we show that Irgm1 also regulated the survival of mature effector CD4+ T lymphocytes by protecting them from IFN-γ-induced autophagic cell death. Mice deficient in both IFN- and Irgm1 were 'rescued' from the lymphocyte depletion and greater mortality that occurs in mice singly deficient in Irgm1 after mycobacterial infection. Our studies identify a feedback mechanism in the T helper type 1 response that limits the detrimental effects of IFN-γ on effector T lymphocyte survival while promoting the antimicrobial functions of IFN-γ.
1 Laboratory of Parasitic Diseases, Bethesda, Maryland 20892, USA.
2 Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA.
3 National Human Genome Research Institute, Bethesda, Maryland 20892, USA.
4 Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
5 Baylor Institute for Immunology Research, Dallas, Texas 75204, USA.
6 These authors contributed equally to this work.
