Schneck J, Maloy W L, Coligan J E, Margulies D H
Molecular Biology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Cell. 1989 Jan 13;56(1):47-55. doi: 10.1016/0092-8674(89)90982-3.
To investigate the molecular basis of the interaction between the T cell receptor and the MHC class I antigen in an allogeneic response, a soluble counterpart of the murine class I molecule, H-2Kb, was genetically engineered. Cells secreting this soluble molecule, H-2Kb/Q10b, inhibited stimulation of an H-2Kb-reactive T cell hybridoma by cells transfected with H-2Kbm10, a weak stimulus, but not by H-2Kb- or H-2Kbm6-transfected cells. Soluble purified H-2Kb/Q10b protein also blocked T cell stimulation. In addition, a peptide from the wild-type H-2Kb molecule spanning the region of the bm10 mutation specifically inhibited activation of the T cell hybridoma by H-2Kbm10 cells, thus suggesting that amino acid residues 163-174 of H-2Kb define a region important for T cell receptor binding. An estimate for the Kd of the T cell receptor for soluble H-2Kb/Q10b was 10(-7) M, while the Kd for soluble peptide 163-174 was 10(-4) M.
为了研究在同种异体反应中T细胞受体与I类主要组织相容性复合体（MHC）抗原之间相互作用的分子基础，对小鼠I类分子H-2Kb的可溶性对应物进行了基因工程改造。分泌这种可溶性分子H-2Kb/Q10b的细胞抑制了用弱刺激物H-2Kbm10转染的细胞对H-2Kb反应性T细胞杂交瘤的刺激，但不抑制用H-2Kb或H-2Kbm6转染的细胞的刺激。可溶性纯化的H-2Kb/Q10b蛋白也阻断了T细胞刺激。此外，来自野生型H-2Kb分子跨越bm10突变区域的一种肽特异性抑制了H-2Kbm10细胞对T细胞杂交瘤的激活，因此表明H-2Kb的163-174位氨基酸残基定义了一个对T细胞受体结合很重要的区域。可溶性H-2Kb/Q10b与T细胞受体的解离常数（Kd）估计为10^(-7) M，而可溶性肽163-174的Kd为10^(-4) M。
