Becker Samuel H, Ronayne Christine E, Bold Tyler D, Jenkins Marc K
bioRxiv. 2024 Aug 23:2024.08.22.609198. doi: 10.1101/2024.08.22.609198.
IFN-γ-producing CD4 T cells are required for protection against lethal ( ) infections. However, the ability of CD4 T cells to suppress growth cannot be fully explained by IFN-γ or other known T cell products. In this study, we show that CD4 T cell-derived IFN-γ promoted the recruitment of monocyte-derived macrophages (MDMs) to the lungs of -infected mice. Although the recruited MDMs became quickly and preferentially infected with , CD4 T cells rapidly disinfected the MDMs. Clearance of from MDMs was not explained by IFN-γ, but rather by MHCII-mediated cognate interactions with CD4 T cells. These interactions promoted MDM expression of glycolysis genes essential for control. Thus, by recruiting MDMs, CD4 T cells initiate a cycle of bacterial phagocytosis, antigen presentation and disinfection in an attempt to clear the bacteria from the lungs.
产生干扰素-γ的CD4 T细胞是抵御致死性（ ）感染所必需的。然而，CD4 T细胞抑制（ ）生长的能力不能完全用干扰素-γ或其他已知的T细胞产物来解释。在本研究中，我们发现CD4 T细胞衍生的干扰素-γ促进单核细胞来源的巨噬细胞（MDM）募集到感染（ ）的小鼠肺部。尽管募集到的MDM很快且优先被（ ）感染，但CD4 T细胞能迅速清除MDM中的（ ）。MDM中（ ）的清除不是由干扰素-γ介导的，而是由MHCII介导的与CD4 T细胞的同源相互作用所致。这些相互作用促进了MDM中对（ ）控制至关重要的糖酵解基因的表达。因此，通过募集MDM，CD4 T细胞启动了一个细菌吞噬、抗原呈递和清除的循环，试图从肺部清除细菌。
