Department of Immunology, Faculty of Medicine, Academic Assembly, University of Toyama, Toyama 930-0194, Japan.
Center for Advanced Antibody Drug Development, University of Toyama, Toyama 930-0194, Japan.
Cells. 2024 Oct 16;13(20):1711. doi: 10.3390/cells13201711.
The MHC class I-related 1 (MR1) molecule is a non-polymorphic antigen-presenting molecule that presents several metabolites to MR1-restricted T cells, including mucosal-associated invariant T (MAIT) cells. MR1 ligands bind to MR1 molecules by forming a Schiff base with the K43 residue of MR1, which induces the folding of MR1 and its reach to the cell surface. An antagonistic MR1 ligand, Ac-6-FP, and the K43A mutation of MR1 are known to inhibit the responses of MR1-restricted T cells. In this study, we analyzed MR1-restricted TCRs obtained from tumor-infiltrating lymphocytes (TILs) from breast cancer patients. They responded to two breast cancer cell lines independently from microbial infection and did not respond to other cancer cell lines or normal breast cells. Interestingly, the reactivity of these TCRs was not inhibited by Ac-6-FP, while it was attenuated by the K43A mutation of MR1. Our findings suggest the existence of a novel class of MR1-restricted TCRs whose antigen is expressed in some breast cancer cells and binds to MR1 depending on the K43 residue of MR1 but without being influenced by Ac-6-FP. This work provides new insight into the physiological roles of MR1 and MR1-restricted T cells.
MHC Ⅰ类相关基因 1(MR1)分子是一种非多态性的抗原呈递分子,可将几种代谢物呈递给 MR1 限制性 T 细胞,包括黏膜相关不变 T(MAIT)细胞。MR1 配体通过与 MR1 的 K43 残基形成席夫碱与 MR1 结合,从而诱导 MR1 的折叠及其到达细胞表面。已知拮抗的 MR1 配体 Ac-6-FP 和 MR1 的 K43A 突变会抑制 MR1 限制性 T 细胞的反应。在这项研究中,我们分析了来自乳腺癌患者肿瘤浸润淋巴细胞(TIL)的 MR1 限制性 TCR。它们独立于微生物感染对两种乳腺癌细胞系产生反应,而对其他癌细胞系或正常乳腺细胞没有反应。有趣的是,这些 TCR 的反应不受 Ac-6-FP 抑制,而受 MR1 的 K43A 突变减弱。我们的发现表明存在一种新型的 MR1 限制性 TCR 类,其抗原在一些乳腺癌细胞中表达,并根据 MR1 的 K43 残基与 MR1 结合,但不受 Ac-6-FP 的影响。这项工作为 MR1 和 MR1 限制性 T 细胞的生理作用提供了新的见解。