Beck B N, Nelson P A, Fathman C G
J Exp Med. 1983 May 1;157(5):1396-404. doi: 10.1084/jem.157.5.1396.
The experiments presented in this study demonstrate that there exist at least two functional epitopes on an I-A molecule that can be recognized by T cell clones. By comparing the abilities of spleen cells from C57BL/6 mice and the congenic I-A mutant line B6.C-H-2bm12 to stimulate alloreactive T cell clones specific for the I-Ab molecule, we have discriminated two sets of clones, those recognizing the I-Ab and I-Abm12 molecule equally well and those able to recognize only the I-Ab molecule. These results imply that the two sets of clones have different receptors for I-A and that they therefore recognize separate epitopes on the I-A molecule. We have similarly been able to separate T cell clones, both alloreactive and L-glutamic acid60-L-alanine30-L-tyrosine10-reactive, specific for the Ab alpha Ak beta hybrid molecule into two groups based on their ability to recognize bm 12 spleen cells. Although the recognition of bm 12 spleen cells by these clones was unexpected since none of them responds to B6 spleen cells, these data again allow us to conclude that these groups of clones have different receptors for the same I-A molecule and therefore that they recognize distinct epitopes on the molecule. Additional studies, in which monoclonal anti-I-A antibodies were used to block the stimulation of T cells by stimulator or antigen-presenting cells, have demonstrated that this blockade can be a steric effect and therefore is not necessarily indicative of direct competition between the antibody and the T cell for the same site on an I-A molecule. Although this study does not reveal the physical nature of an I region-controlled "antigen-restriction site," we can suggest that increasing the number of possible functional Ia restriction sites either through combinatorial association of alpha and beta chains or by using more than one site per molecule will increase the number of configurations the ternary complex of Ia, antigen and T cell receptor(s) can form.
本研究中展示的实验表明,I-A分子上至少存在两个可被T细胞克隆识别的功能性表位。通过比较C57BL/6小鼠的脾细胞和同基因I-A突变系B6.C-H-2bm12刺激针对I-Ab分子的同种异体反应性T细胞克隆的能力,我们区分出两组克隆,一组对I-Ab和I-Abm12分子识别能力相同,另一组只能识别I-Ab分子。这些结果意味着这两组克隆对I-A具有不同的受体,因此它们识别I-A分子上不同的表位。我们同样能够根据其识别bm 12脾细胞的能力,将针对AbαAkβ杂合分子的同种异体反应性和L-谷氨酸60-L-丙氨酸30-L-酪氨酸10反应性的T细胞克隆分为两组。尽管这些克隆对bm 12脾细胞的识别出乎意料,因为它们都不响应B6脾细胞,但这些数据再次使我们得出结论,这些克隆组对同一I-A分子具有不同的受体,因此它们识别该分子上不同的表位。另外的研究使用单克隆抗I-A抗体来阻断刺激细胞或抗原呈递细胞对T细胞的刺激,结果表明这种阻断可能是一种空间效应,因此不一定表明抗体与T细胞在I-A分子上的同一位点存在直接竞争。尽管本研究没有揭示I区控制的“抗原限制位点”的物理性质,但我们可以提出,通过α链和β链的组合关联或每个分子使用多个位点来增加可能的功能性Ia限制位点的数量,将增加Ia、抗原和T细胞受体三元复合物能够形成的构型数量。