干擾素γ是一種抗菌信號(hào)蛋白質(zhì),?？茖W(xué)家們發(fā)現(xiàn)一種分子,，它能在干擾素γ大量出現(xiàn)時(shí)保護(hù)激活的免疫細(xì)胞,，讓它們得以生存,。 他們?cè)谛鲁霭娴摹蹲匀?mdash;免疫學(xué)》期刊中報(bào)告說(shuō)，在慢性感染出現(xiàn)時(shí)免疫能持續(xù)作出反應(yīng),，Irgm1分子發(fā)揮了關(guān)鍵作用,。慢性免疫反應(yīng)出現(xiàn)在許多種類(lèi)的寄生蟲(chóng)疾病中。
干擾素是一種抗菌化合物,，有助于病毒和其他細(xì)胞病原菌的根除,。但高濃度的干擾素對(duì)附近的細(xì)胞卻是有毒的。因此,，這是一個(gè)困境：制造干擾素應(yīng)對(duì)感染的免疫細(xì)胞在這一過(guò)程中如何保全自己,？
Carl Feng和同事鑒別出一種名為Irgm1 的分子，它在保護(hù)生產(chǎn)干擾素的免疫細(xì)胞免遭其毒素中毒的過(guò)程中發(fā)揮了關(guān)鍵作用,。他們指出,，面對(duì)干擾素γ時(shí)，缺失 Irgm1的小鼠免疫細(xì)胞無(wú)法增生,，并進(jìn)入一種名為凋亡的細(xì)胞自殺過(guò)程,。免疫細(xì)胞的減少導(dǎo)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又缺乏干擾素γ的小鼠卻存活下來(lái)了,，表明Irgm1保護(hù)了這些免疫細(xì)胞不受干擾素γ毒性的影響。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
