Masaki H, Irimajiri K, Horiuchi A, Yamaguchi J, Toyosaki T, Suzuki R, Kurane I
Department of Microbiology, Kinki University School of Medicine, Osaka, Japan.
Cell Immunol. 1996 Dec 15;174(2):180-9. doi: 10.1006/cimm.1996.0308.
It is known that anti-alpha(1 --> 3) dextran antibodies of BALB/c mice are ordinarily of distinctive idiotypes (Id), one of which is the individual idiotype (IdI) that is represented by J558 or M104E to myeloma protein. In the present study, we established T cell line of Th1 type which recognized the Id of anti-alpha(1 --> 3) dextran antibody, and investigated its specificity and functions. The T cell line, named J-2R, had a phenotype of CD3+ CD4+ CD8- and expressed alphabeta-T cell receptors (TcR). J-2R proliferated in response to J558 in an I-Ed-restricted manner but did not respond to M104E which had substitution at amino acids 100 and 101. We confirmed that J-2R recognized J558 IdI, using synthetic peptides corresponding to two serial amino acid residues, Arg100 and Tyr101, spanning the J558 IdI in the third hypervariable region (hv3) of the heavy chain. alpha(1 --> 3) dextran-binding B cells which were isolated from dextran-immunized mice activated J-2R, but B cells from nonimmune mice did not. J-2R produced IL-2, IFN-gamma and IL-6, but did not produce IL-4, IL-5, or IL-10. Furthermore, J-2R inhibited the growth of J558 myeloma cells inoculated to the syngeneic mice in vivo. These findings suggest that Id-specific CD4+ T cells, J-2R, are involved in Id network and may play a role in vivo. J-2R is useful for analysis of the role of the Id-specific helper T cells in immune network because J558 IdI is frequently present on anti-alpha(1 --> 3) dextran antibodies.
已知BALB/c小鼠的抗α(1→3)葡聚糖抗体通常具有独特的个体基因型(Id),其中之一是由骨髓瘤蛋白J558或M104E所代表的个体基因型(IdI)。在本研究中,我们建立了识别抗α(1→3)葡聚糖抗体Id的Th1型T细胞系,并研究了其特异性和功能。该T细胞系名为J-2R,具有CD3+ CD4+ CD8-的表型,并表达αβ-T细胞受体(TcR)。J-2R以I-Ed限制的方式对J558产生增殖反应,但对在氨基酸100和101处有替换的M104E无反应。我们使用与重链第三高变区(hv3)中跨越J558 IdI的两个连续氨基酸残基Arg100和Tyr101对应的合成肽,证实J-2R识别J558 IdI。从葡聚糖免疫小鼠中分离出的α(1→3)葡聚糖结合B细胞激活了J-2R,但来自非免疫小鼠的B细胞则不能。J-2R产生IL-2、IFN-γ和IL-6,但不产生IL-4、IL-5或IL-10。此外,J-2R在体内抑制了接种到同基因小鼠体内的J558骨髓瘤细胞的生长。这些发现表明,Id特异性CD4+ T细胞J-2R参与Id网络,可能在体内发挥作用。J-2R对于分析Id特异性辅助性T细胞在免疫网络中的作用很有用,因为J558 IdI经常存在于抗α(1→3)葡聚糖抗体上。