The location of intraepithelial lymphocytes (IEL) between epithelial cells, their effector memory, cytolytic and inflammatory phenotype positions them to kill infected epithelial cells and protect the intestine against pathogens. Human TCRαβ⁺CD8αβ⁺ IEL have the dual capacity to recognize modified self via natural killer (NK) receptors (autoreactivity) as well as foreign antigen via the T cell receptor (TCR), which is accomplished in mouse by two cell subsets, the naturally occurring TCRαβ⁺CD8αα⁺ and adaptively induced TCRαβ⁺CD8αβ⁺ IEL subsets, respectively. The private/oligoclonal nature of the TCR repertoire of both human and mouse IEL suggests local environmental factors dictate the specificity of IEL responses. The line between sensing of foreign antigens and autoreactivity is blurred for IEL in celiac disease, where recognition of stress ligands by induced activating NK receptors in conjunction with inflammatory signals such as IL-15 can result in low-affinity TCR/non-cognate antigen and NK receptor/stress ligand interactions triggering destruction of intestinal epithelial cells.

中文翻译：

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人上皮内淋巴细胞。

上皮细胞之间的上皮内淋巴细胞 (IEL) 的位置、它们的效应记忆、细胞溶解和炎症表型使它们能够杀死受感染的上皮细胞并保护肠道免受病原体侵害。人类TCRαβ ⁺ CD8αβ ⁺ IEL 具有通过自然杀伤 (NK) 受体（自身反应性）识别修饰的自身以及通过 T 细胞受体 (TCR) 识别外来抗原的双重能力，这在小鼠中由两个细胞亚群完成，自然发生TCRαβ ^{+ CD8αα +}和适应性诱导的TCRαβ ⁺ CD8αβ ⁺IEL子集，分别。人类和小鼠 IEL 的 TCR 库的私有/寡克隆性质表明，当地环境因素决定了 IEL 反应的特异性。对于乳糜泻中的 IEL，外来抗原的感知与自身反应之间的界限模糊，其中通过诱导激活 NK 受体结合炎症信号（如 IL-15）识别应激配体可导致低亲和力 TCR/非同源抗原和NK 受体/应激配体相互作用触发肠上皮细胞的破坏。