Speck N A, Pierce S K
J Exp Med. 1982 Feb 1;155(2):574-86. doi: 10.1084/jem.155.2.574.
Previous studies have demonstrated that the B cells in immune and nonimmune mice manifest different major histocompatibility complex (MHC) collaborative phenotypes with antigen-specific T cells. Immune, or secondary B cells require syngeneic-like MHC recognition by collaborating T cells, and in its absence fail to be stimulated. Primary B cells manifest a much less stringent requisite for MHC recognition by T cells, and under conditions in which secondary B cells fail to be stimulated, primary B cells are stimulated to secrete IgM antibody. Experiments were conducted to determine whether the acquisition of the secondary B cells' MHC collaborative phenotype was dependent on the presence of T cells during in vivo immunization. B cell populations from T dependently and T independently immunized conventional BALB/c and athymic BALB/c nu/nu mice were compared in their ability to collaborate with allogeneic T cells. Although antigen alone promotes the differentiation of several secondary B cell characteristics, including an increase in the frequency of antigen-specific B cells and a preference for IgG1 antibody synthesis in vitro, the acquisition of the secondary B cells' MHC collaborative phenotype was dependent on the presence of T cells during in vivo immunization. B cell populations from T dependently and T independently immunized conventional BALB/c and athymic BALB/c nu/nu mice were compared in their ability to collaborate with allogeneic T cells. Although antigen alone promotes the differentiation of several secondary B cell characteristics, including an increase in the frequency of antigen-specific B cells and a preference of IgG1 antibody synthesis in vitro, the acquisition of the secondary B cells' MHC collaborative phenotype was found to be dependent on the presence of T cells during in vivo immunization. Thus, the restriction imposed on T cell-B-cell-collaborative interactions in secondary humoral immune responses appears to be the result of T dependent antigen-driven events.
先前的研究表明，免疫小鼠和非免疫小鼠中的B细胞与抗原特异性T细胞表现出不同的主要组织相容性复合体（MHC）协作表型。免疫B细胞或次级B细胞需要协作T细胞进行同基因样MHC识别，否则无法被刺激。初级B细胞对T细胞识别MHC的要求则宽松得多，在次级B细胞无法被刺激的条件下，初级B细胞会被刺激分泌IgM抗体。开展实验以确定次级B细胞MHC协作表型的获得是否依赖于体内免疫期间T细胞的存在。比较了来自T细胞依赖型和T细胞非依赖型免疫的常规BALB/c小鼠和无胸腺BALB/c nu/nu小鼠的B细胞群体与同种异体T细胞协作的能力。尽管单独的抗原可促进几种次级B细胞特征的分化，包括抗原特异性B细胞频率的增加以及体外对IgG1抗体合成的偏好，但次级B细胞MHC协作表型的获得依赖于体内免疫期间T细胞的存在。比较了来自T细胞依赖型和T细胞非依赖型免疫的常规BALB/c小鼠和无胸腺BALB/c nu/nu小鼠的B细胞群体与同种异体T细胞协作的能力。尽管单独的抗原可促进几种次级B细胞特征的分化，包括抗原特异性B细胞频率的增加以及体外对IgG1抗体合成的偏好，但发现次级B细胞MHC协作表型的获得依赖于体内免疫期间T细胞的存在。因此，在次级体液免疫反应中对T细胞 - B细胞协作相互作用施加的限制似乎是T细胞依赖型抗原驱动事件的结果。
