Innate (-like) T lymphocytes such as natural killer T (NKT) cells play a pivotal role in the recognition of microbial infections and their subsequent elimination. They frequently localize to potential sites of pathogen entry at which they survey extracellular and intracellular tissue spaces for microbial antigens. Engagement of their T cell receptors (TCRs) induces an explosive release of different cytokines and chemokines, which often pre-exist as constitutively expressed gene transcripts in NKT cells and underlie their poised effector state. Thus, NKT cells regulate immune cell migration and activation and subsequently, bridge innate and adaptive immune responses. In contrast to conventional T cells, which react to peptide antigens, NKT cells recognize lipids presented by the MHC class I like CD1d molecule on antigen presenting cells (APCs). Furthermore, each NKT cell TCR can recognize various antigen specificities, whereas a conventional T lymphocyte TCR reacts mostly only to one single antigen. These lipid antigens are either intermediates of the intracellular APC`s-own metabolism or originate from the cell wall of different bacteria, fungi or protozoan parasites. The best-characterized subset, the type 1 NKT cell subset expresses a semi-invariant TCR. In contrast, the TCR repertoire of type 2 NKT cells is diverse. Furthermore, NKT cells express a panoply of inhibitory and activating NK cell receptors (NKRs) that contribute to their primarily TCR-mediated rapid, innate like immune activation and even allow an adaption of their immune response in an adoptive like manner. Dueto their primary localization at host-environment interfaces, NKT cells are one of the first immune cells that interact with signals from different microbial pathogens. Vice versa, the mutual exchange with local commensal microbiota shapes also the biology of NKT cells, predominantly in the gastrointestinal tract. Following infection, two main signals drive the activation of NKT cells: first, cognate activation upon TCR ligation by microbial or endogenous lipid antigens; and second, bystander activation due to cytokines. Here we will discuss the role of NKT cells in the control of different microbial infections comparing pathogens expressing lipid ligands in their cell walls to infectious agents inducing endogenous lipid antigen presentation by APCs.

先天性（样）T 淋巴细胞，如自然杀伤 T (NKT) 细胞，在识别微生物感染及其随后的消除方面发挥着关键作用。他们经常定位在病原体进入的潜在位点，在那里他们调查微生物抗原的细胞外和细胞内组织空间。它们的 T 细胞受体 (TCR) 的参与诱导了不同细胞因子和趋化因子的爆炸性释放，这些细胞因子和趋化因子通常预先存在于 NKT 细胞中作为组成型表达的基因转录本，并成为其稳定效应状态的基础。因此，NKT 细胞调节免疫细胞迁移和激活，并随后桥接先天性和适应性免疫反应。与与肽抗原反应的常规 T 细胞相反，NKT 细胞识别由 MHC I 类呈递的脂质，如抗原呈递细胞 (APC) 上的 CD1d 分子。此外，每个 NKT 细胞 TCR 可以识别各种抗原特异性，而传统的 T 淋巴细胞 TCR 主要只对一种单一抗原反应。这些脂质抗原要么是细胞内 APC 自身代谢的中间体，要么来自不同细菌、真菌或原生动物寄生虫的细胞壁。表征最好的子集，1 型 NKT 细胞子集表示半不变的 TCR。相比之下，2 型 NKT 细胞的 TCR 库是多种多样的。此外，NKT 细胞表达一整套抑制性和激活性 NK 细胞受体 (NKR)，这有助于它们主要由 TCR 介导的快速、先天性免疫激活，甚至允许以过继性方式适应它们的免疫反应。由于它们主要定位于主机环境接口，NKT 细胞是最早与来自不同微生物病原体的信号相互作用的免疫细胞之一。反之亦然，与局部共生微生物群的相互交换也塑造了 NKT 细胞的生物学，主要在胃肠道中。感染后，有两个主要信号驱动 NKT 细胞的激活：第一，微生物或内源性脂质抗原在 TCR 连接时的同源激活；其次，由于细胞因子的旁观者激活。在这里，我们将讨论 NKT 细胞在控制不同微生物感染中的作用，将在其细胞壁中表达脂质配体的病原体与通过 APC 诱导内源性脂质抗原呈递的感染因子进行比较。主要在胃肠道。感染后，有两个主要信号驱动 NKT 细胞的激活：第一，微生物或内源性脂质抗原在 TCR 连接时的同源激活；其次，由于细胞因子的旁观者激活。在这里，我们将讨论 NKT 细胞在控制不同微生物感染中的作用，将在其细胞壁中表达脂质配体的病原体与通过 APC 诱导内源性脂质抗原呈递的感染因子进行比较。主要在胃肠道。感染后，有两个主要信号驱动 NKT 细胞的激活：第一，微生物或内源性脂质抗原在 TCR 连接时的同源激活；第二，由细胞因子引起的旁观者激活。在这里，我们将讨论 NKT 细胞在控制不同微生物感染中的作用，将在其细胞壁中表达脂质配体的病原体与通过 APC 诱导内源性脂质抗原呈递的感染因子进行比较。