Howard Hughes Medical Institute, National Jewish Health, Denver, CO 80206, USA.
Proc Natl Acad Sci U S A. 2012 Nov 6;109(45):18517-22. doi: 10.1073/pnas.1215928109. Epub 2012 Oct 22.
T cell-mediated allergy to Ni(++) is one of the most common forms of allergic contact dermatitis, but how the T-cell receptor (TCR) recognizes Ni(++) is unknown. We studied a TCR from an allergic patient that recognizes Ni(++) bound to the MHCII molecule DR52c containing an unknown self-peptide. We identified mimotope peptides that can replace both the self-peptide and Ni(++) in this ligand. They share a p7 lysine whose εNH(2) group is surface-exposed when bound to DR52c. Whereas the TCR uses germ-line complementary-determining region (CDR)1/2 amino acids to dock in the conventional diagonal mode on the mimotope-DR52c complex, the interface is dominated by the TCR Vβ CDR3 interaction with the p7 lysine. Mutations in the TCR CDR loops have similar effects on the T-cell response to either the mimotope or Ni(++) ligand. We suggest that the mimotope p7 lysine mimics Ni(++) in the natural TCR ligand and that MHCII β-chain flexibility in the area around the peptide p7 position forms a common site for cation binding in metal allergies.
T 细胞介导的对 Ni(++)的过敏反应是最常见的过敏接触性皮炎形式之一,但 T 细胞受体 (TCR) 如何识别 Ni(++)尚不清楚。我们研究了一种来自过敏患者的 TCR,该 TCR 识别与 MHCII 分子 DR52c 结合的 Ni(++),其中包含一个未知的自身肽。我们鉴定了可以替代配体中自身肽和 Ni(++)的模拟肽。它们共享一个 p7 赖氨酸,当与 DR52c 结合时,其 εNH(2)基团暴露在表面。虽然 TCR 使用种系互补决定区 (CDR)1/2 氨基酸以传统的对角模式在模拟肽-DR52c 复合物上对接,但界面主要由 TCR Vβ CDR3 与 p7 赖氨酸的相互作用主导。TCR CDR 环中的突变对模拟肽或 Ni(++)配体的 T 细胞反应具有相似的影响。我们认为模拟肽 p7 赖氨酸模拟了天然 TCR 配体中的 Ni(++),并且肽 p7 位置周围 MHCII β 链的灵活性形成了金属过敏中阳离子结合的共同位点。