7F5K
Crystal structure of TCR4-1 ectodomain
7F5K の概要
エントリーDOI | 10.2210/pdb7f5k/pdb |
分子名称 | T cell receptor alpha chain, T cell receptor beta chain (2 entities in total) |
機能のキーワード | t-cell receptor, ectodomain, immune system |
由来する生物種 | Mus musculus 詳細 |
タンパク質・核酸の鎖数 | 4 |
化学式量合計 | 96972.04 |
構造登録者 | |
主引用文献 | Shibata, K.,Motozono, C.,Nagae, M.,Shimizu, T.,Ishikawa, E.,Motooka, D.,Okuzaki, D.,Izumi, Y.,Takahashi, M.,Fujimori, N.,Wing, J.B.,Hayano, T.,Asai, Y.,Bamba, T.,Ogawa, Y.,Furutani-Seiki, M.,Shirai, M.,Yamasaki, S. Symbiotic bacteria-dependent expansion of MR1-reactive T cells causes autoimmunity in the absence of Bcl11b. Nat Commun, 13:6948-6948, 2022 Cited by PubMed Abstract: MHC class I-related protein 1 (MR1) is a metabolite-presenting molecule that restricts MR1-reactive T cells including mucosal-associated invariant T (MAIT) cells. In contrast to MAIT cells, the function of other MR1-restricted T cell subsets is largely unknown. Here, we report that mice in which a T cell-specific transcription factor, B-cell lymphoma/leukemia 11B (Bcl11b), was ablated in immature thymocytes (Bcl11b mice) develop chronic inflammation. Bcl11b mice lack conventional T cells and MAIT cells, whereas CD4IL-18R αβ T cells expressing skewed Traj33 (Jα33) T cell receptors (TCR) accumulate in the periphery, which are necessary and sufficient for the pathogenesis. The disorders observed in Bcl11b mice are ameliorated by MR1-deficiency, transfer of conventional T cells, or germ-free conditions. We further show the crystal structure of the TCR expressed by Traj33 T cells expanded in Bcl11b mice. Overall, we establish that MR1-reactive T cells have pathogenic potential. PubMed: 36376329DOI: 10.1038/s41467-022-34802-8 主引用文献が同じPDBエントリー |
実験手法 | X-RAY DIFFRACTION (3.00002976572 Å) |
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