Saunders B M, Zhan Y, Cheers C
Department of Microbiology, University of Melbourne, Parkville, Victoria, Australia.
Infect Immun. 1995 Oct;63(10):4011-5. doi: 10.1128/iai.63.10.4011-4015.1995.
Acquired cellular resistance against Mycobacterium avium complex (MAC) infections involves the induction of Th1 type gamma interferon (IFN-gamma)-producing T cells. Interleukin-12 (IL-12) is a cytokine involved in the control of IFN-gamma production by T cells and NK cells. The role of IL-12 in the response to MAC infection was investigated. Depletion of endogenous IL-12 by injection of monoclonal antibody prior to and during intranasal infection with MAC resulted in an 150- to 550-fold increase in bacterial load in lung, spleen, and liver homogenates by 10 weeks postinfection. Depletion of IL-12 abrogated the ability of spleen cell cultures to produce IFN-gamma in response to stimulus with live MAC. IL-12-depleted mice showed a 75% decrease in the number of inflammatory cells entering the lungs following intranasal infection with MAC, with significant reductions in cytotoxic activity and nitric oxide production by lung cells. This work suggests that IL-12 plays a major role in the activation of IFN-gamma-producing cells during MAC infection.
获得性细胞对鸟分枝杆菌复合群（MAC）感染的抗性涉及诱导产生Th1型γ干扰素（IFN-γ）的T细胞。白细胞介素-12（IL-12）是一种参与T细胞和NK细胞控制IFN-γ产生的细胞因子。研究了IL-12在对MAC感染反应中的作用。在鼻内感染MAC之前和期间注射单克隆抗体以耗尽内源性IL-12，导致感染后10周时肺、脾和肝匀浆中的细菌载量增加150至550倍。耗尽IL-12消除了脾细胞培养物在受到活MAC刺激时产生IFN-γ的能力。IL-12耗尽的小鼠在鼻内感染MAC后进入肺部的炎性细胞数量减少了75%，肺细胞的细胞毒性活性和一氧化氮产生显著降低。这项研究表明，IL-12在MAC感染期间激活产生IFN-γ的细胞中起主要作用。
