Takahashi Y, Ametani A, Totsuka M, Fujine K, Tsuji N M, Kurisaki J, Kaminogawa S
Department of Applied Biological Chemistry, The University of Tokyo, Japan.
Immunol Lett. 1998 Apr;61(2-3):97-101. doi: 10.1016/s0165-2478(98)00002-9.
We have examined whether the interaction of peptide-loaded MHC molecules on the surface of B-cells with antigen-specific T-cell receptors (TCRs) enhances Ig secretion in the presence of other antigen-independent interactions in vitro. B-cells specific for region 25-40 of beta-lactoglobulin (beta-LG) were stimulated in a T-cell dependent manner using plasma membranes (PM) derived from two different T-helper (Th) clones, culture supernatants of activated Th2 cells and beta-LG as a specific antigen. PM were obtained from either the beta-LG-specific T-cell clone H1.1 which can mediate specific TCR/MHC class II interactions as well as antigen-independent ones or from the D10 clone which bears a TCR of an irrelevant specificity and thus, can only mediate antigen-independent interactions. IgG, but not IgM, secretion was specifically enhanced by H1.1 PM, but not D10 PM in the presence of beta-LG. Furthermore, a blockade of TCR/MHC class II interactions using either anti-T-cell receptor, beta or anti-CD4 monoclonal antibodies inhibited this enhanced IgG secretion in response to beta-LG. The results show that while antigen-independent interactions between T- and B-cells can enhance secretion of IgM antibodies, specific interactions between TCRs and peptide:MHC complexes stimulate B-cells to enhance secretion of IgG but not IgM antibodies. This mechanism may contribute to antibody secretion only from B-cells activated through cognate interaction in vivo.
我们研究了在体外存在其他非抗原依赖性相互作用的情况下，B细胞表面负载肽的MHC分子与抗原特异性T细胞受体（TCR）的相互作用是否会增强Ig分泌。使用源自两种不同T辅助（Th）克隆的质膜（PM）、活化Th2细胞的培养上清液以及β-乳球蛋白（β-LG）作为特异性抗原，以T细胞依赖性方式刺激对β-LG 25-40区域具有特异性的B细胞。PM取自β-LG特异性T细胞克隆H1.1，其可介导特异性TCR/MHC II类相互作用以及非抗原依赖性相互作用，或者取自D10克隆，其携带不相关特异性的TCR，因此只能介导非抗原依赖性相互作用。在存在β-LG的情况下，H1.1 PM特异性增强了IgG而非IgM的分泌，而D10 PM则没有。此外，使用抗T细胞受体β或抗CD4单克隆抗体阻断TCR/MHC II类相互作用可抑制对β-LG的这种增强的IgG分泌。结果表明，虽然T细胞和B细胞之间的非抗原依赖性相互作用可增强IgM抗体的分泌，但TCR与肽：MHC复合物之间的特异性相互作用刺激B细胞增强IgG而非IgM抗体的分泌。这种机制可能仅有助于体内通过同源相互作用激活的B细胞的抗体分泌。
