Dorner Brigitte G, Smith Hamish R C, French Anthony R, Kim Sungjin, Poursine-Laurent Jennifer, Beckman Diana L, Pingel Jeanette T, Kroczek Richard A, Yokoyama Wayne M
Howard Hughes Medical Institute and Division of Rheumatology, Department of Medicine, Washington University School of Medicine and Barnes-Jewish Hospital, St. Louis, MO 63110, USA.
J Immunol. 2004 Mar 1;172(5):3119-31. doi: 10.4049/jimmunol.172.5.3119.
Cytokines and chemokines activate and direct effector cells during infection. We previously identified a functional group of five cytokines and chemokines, namely, IFN-gamma, activation-induced T cell-derived and chemokine-related cytokine/lymphotactin, macrophage-inflammatory protein 1alpha, macrophage-inflammatory protein 1beta, and RANTES, coexpressed in individual activated NK cells, CD8(+) T cells, and CD4(+) Th1 cells in vitro and during in vivo infections. However, the stimuli during infection were not known. In murine CMV (MCMV) infection, the DAP12/KARAP-associated Ly49H NK cell activation receptor is crucial for resistance through recognition of MCMV-encoded m157 but NK cells also undergo in vivo nonspecific responses to uncharacterized stimuli. In this study, we show that Ly49H ligation by m157 resulted in a coordinated release of all five cytokines/chemokines from Ly49H(+) NK cells. Whereas other cytokines also triggered the release of these cytokines/chemokines, stimulation was not confined to the Ly49H(+) population. At the single-cell level, the production of the five mediators showed strong positive correlation with each other. Interestingly, NK cells were a major source of these five cytokines/chemokines in vitro and in vivo, whereas infected macrophages produced only limited amounts of macrophage-inflammatory protein 1alpha, macrophage-inflammatory protein1beta, and RANTES. These findings suggest that both virus-specific and nonspecific NK cells play crucial roles in activating and directing other inflammatory cells during MCMV infection.
细胞因子和趋化因子在感染过程中激活并引导效应细胞。我们之前鉴定出一组由五种细胞因子和趋化因子组成的功能群,即干扰素-γ、活化诱导的T细胞衍生的与趋化因子相关的细胞因子/淋巴细胞趋化因子、巨噬细胞炎性蛋白1α、巨噬细胞炎性蛋白1β和调节激活正常T细胞表达和分泌的因子,它们在体外及体内感染期间在单个活化的自然杀伤(NK)细胞、CD8(+) T细胞和CD4(+) Th1细胞中共同表达。然而,感染期间的刺激因素尚不清楚。在小鼠巨细胞病毒(MCMV)感染中,与DAP12/KARAP相关的Ly49H NK细胞活化受体通过识别MCMV编码的m157对抵抗感染至关重要,但NK细胞也会对未明确的刺激产生体内非特异性反应。在本研究中,我们发现m157与Ly49H结合导致Ly49H(+) NK细胞协调释放所有这五种细胞因子/趋化因子。虽然其他细胞因子也能触发这些细胞因子/趋化因子的释放,但刺激并不局限于Ly49H(+)群体。在单细胞水平上,这五种介质的产生彼此之间呈现出强烈的正相关。有趣的是,NK细胞在体外和体内都是这五种细胞因子/趋化因子的主要来源,而受感染的巨噬细胞仅产生有限量的巨噬细胞炎性蛋白1α、巨噬细胞炎性蛋白1β和调节激活正常T细胞表达和分泌的因子。这些发现表明,在MCMV感染期间,病毒特异性和非特异性NK细胞在激活和引导其他炎性细胞方面都起着关键作用。