SUBSETS OF HELPER T CELLS IN IMMUNE REGULATION

我们先前描述了诱导大量的 自身反应性T细胞在免疫反应过程中随机选择 外来抗原 这些T细胞似乎是MHC特异性的， 非特异性辅助功能，用于增强增殖， 活化的B细胞的分化。 我们的实验表明 抗原特异性和自身反应性T细胞之间的关系， 体外自身反应性T细胞的初始诱导需要抗原性 再刺激引发的淋巴结细胞。 自身反应性T细胞可以衍生 抗原特异性前体 或者，抗原特异性T细胞 可能需要激活自身反应性T细胞的刺激物。 我们 提出实验来区分这些和其他可能性。 我们选择了自身反应性和抗原特异性T细胞系 从软琼脂中克隆出来的。 一种用于计数前兆的通用方法， 将产生自身反应性T细胞，并进一步产生自身反应性克隆。 分离并表征MHC特异性。 为了确定 自身反应性T细胞克隆的相对异质性， 特异性I-A亚区单倍型，我们将尝试提高抗受体 针对同基因和同种异体的单个克隆的抗体 免疫接种。 正常人自身反应性T细胞的鉴定 个人提出了关于扩大管制的重要问题， 这些T细胞在体内以及它们在表达 自身抗体 我们将首先通过定义任何特殊的 自身反应性T细胞刺激物的需求，一个可能的目标 监管。 此外，我们还将描述体液或细胞 调节机制，可能会激活反复转让， 将自身反应性T细胞的非致瘤性克隆转化为同基因个体。

We have previously described induction of a large population of autoreactive T cells in the course of an immune response to randomly chosen foreign antigens. These T cells appear to be MHC-specific and provide a non-specific helper function that serves to enhance proliferation and differentiation of activated B cells. Our experiments suggest a relationship between antigen-specific and autoreactive T cells in that initial induction of autoreactive T cells in vitro requires antigenic restimulation of primed lymph node cells. Autoreactive T cells may derive from antigen-specific precursors. Alternatively, antigen-specific T cells might be required to activate stimulators of autoreactive T cells. We propose experiments to distinguish between these and other possiblilities. We have selected lines of both autoreactive and antigen-specific T cells from clonies in soft agar. A general method for enumerating precursors to autoreactive T cells will be developed and further autoreactive clones will be isolated and characterized as to MHC-specificity. In order to determine the relative heterogeneity of autoreactive T cell clones directed against a specific I-A subregion haplotype, we will attempt to raise anti-receptor antibodies to individual clones in both syngeneic and allogeneic immunizations. The identification of autoreactive T cells in normal individuals raises important issues concerning regulation of expansion of such T cells in vivo and their possible role in expression of autoantibodies. We will address these issues first by defining any special requirements for stimulators of autoreactive T cells, one possible target of regulation. We will, in addition, characterize humoral or cellular regulatory mechanisms that may be activated by repeated transfers of non-tumorigenic clones of autoreactive T cells into syngeneic individuals.