Pubmed文献速递|人类MAIT细胞缺乏同种异体反应潜能：促使它们成为过继免疫治疗的通用细胞。
背景：黏膜相关不变性T（MAIT）细胞是半不变性T细胞，其识别高度保守的MR1分子呈递的微生物抗原。 MAIT细胞主要位于肝脏和屏障组织中，是抗微生物防御的有效效应物。 MAIT细胞在出生时很少，在婴儿期约6年内逐渐积累。 MAIT细胞的潜在细胞毒性以及它们新近描述的调节和组织修复功能，为在过继治疗中开发其特性提供了可能性。 用作“通用”细胞的先决条件是缺乏同种反应性潜能，这有待证明。
方法：我们使用了离体，体外和体内模型来确定人MAIT细胞是否有助于同种异体反应。
结果：我们表明，同种异体造血干细胞移植后MAIT细胞的恢复概括了它们在儿童早期的缓慢生理扩张，而与常规T细胞的恢复无关。 在体外，同种异体细胞和细胞因子提供的信号不会诱导持续的MAIT细胞增殖。 在体内，在免疫缺陷小鼠的T细胞介导的异种移植物抗宿主病（GVHD）模型中，人MAIT细胞不会在组织中扩增或积累。
结论：总而言之，这些结果提供了证据，表明MAIT细胞没有同种反应性潜能，并为在普遍采用的治疗中克服HLA差异障碍的转化潜能铺平了道路。
Background: Mucosal associated invariant T (MAIT) cells are semi-invariant T cells that recognize microbial antigens presented by the highly conserved MR1 molecule. MAIT cells are predominantly localized in the liver and barrier tissues and are potent effectors of anti-microbial defense. MAIT cells are very few at birth and accumulate gradually over a period of about 6 years during infancy. The cytotoxic potential of MAIT cells, as well as their newly described regulatory and tissue repair functions, open the possibility of exploiting their properties in adoptive therapy. A prerequisite for their use as "universal" cells would be a lack of alloreactive potential, which remains to be demonstrated. Methods: We used ex vivo, in vitro and in vivo models to determine if human MAIT cells contribute to allogeneic responses. Results: We show that recovery of MAIT cells after allogeneic hematopoietic stem cell transplantation recapitulates their slow physiological expansion in early childhood, independent of recovery of conventional T cells. In vitro, signals provided by allogeneic cells and cytokines do not induce sustained MAIT cell proliferation. In vivo, human MAIT cells do not expand nor accumulate in tissues in a model of T-cell mediated xenogeneic graft-versus-host disease (GVHD) in immunodeficient mice. Conclusions: Altogether, these results provide evidence that MAIT cells are devoid of alloreactive potential and pave the way for harnessing their translational potential in universal adoptive therapy overcoming barriers of HLA disparity
doi: https://doi.org/10.1101/2021.04.29.21256184
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