利用HLA - A2突变体研究同种异体反应性。
Alloreactivity studied with mutants of HLA-A2.
作者信息
Santos-Aguado J, Crimmins M A, Mentzer S J, Burakoff S J, Strominger J L
机构信息
Division of Tumor Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
出版信息
Proc Natl Acad Sci U S A. 1989 Nov;86(22):8936-40. doi: 10.1073/pnas.86.22.8936.
Abstract
Based on the crystal structure of HLA-A2.1 and the recognition of a panel of mutant HLA-A2.1 molecules by a large number of alloreactive cytotoxic T lymphocyte clones, a model to explain alloreactivity is described. In this model recognition of an allogeneic major histocompatibility complex molecule by a self-restricted T-cell receptor occurs as the result of accommodation by the receptor of a few amino acid differences in the major histocompatibility complex molecule--i.e., cross-recognition. Alloreactivity is the result of the presence in the foreign antigen binding site of the allogeneic major histocompatibility complex molecule of unusual self-peptides, reactivity to which could not have been eliminated by negative thymic selection.
摘要
基于HLA - A2.1的晶体结构以及大量同种异体反应性细胞毒性T淋巴细胞克隆对一组突变HLA - A2.1分子的识别，描述了一种解释同种异体反应性的模型。在该模型中，自身限制性T细胞受体对同种异体主要组织相容性复合体分子的识别是由于受体适应了主要组织相容性复合体分子中的少数氨基酸差异的结果——即交叉识别。同种异体反应性是由于在同种异体主要组织相容性复合体分子的外来抗原结合位点中存在异常的自身肽，而对这些自身肽的反应性无法通过阴性胸腺选择消除。
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