T-CELL DIFFERENTIATION: MOLECULAR MECHANISMS

本文介绍了调节T细胞分化的各个方面和模型。 已解决。 有证据表明，某些T细胞淋巴瘤克隆是可诱导的， 在体外表达Lyt-1。Lyt-1表达的阻断和伴随的 Ly-5单克隆抗体产生的IL-2和其他数据提示我们， 前Lyl细胞上的Ly-5参与了IL-1依赖性步骤， IL-2的产生和Lyl表型。 我们的目标是描述这一点 在转录和翻译方面的转变。 我们发现，重组γ-干扰素可以诱导Lyb-2， 继之以B谱系细胞的sIg表面表型。 一个特殊的点 有趣的是，这需要的γ-干扰素远少于 常规病毒保护（CPE）测定。 因此γ-干扰素可能 作为淋巴细胞分化剂，即使在 在普通CPE测定不能显示其存在的情况下。 Lyt-1在B细胞亚群中表达的意义以及Ly 1 而Ly 123组T细胞是模糊的。 我们的目标是阐明诱导 我们在有丝分裂原刺激的克隆性B细胞中观察到Lyt-1的增加， 与T细胞相比，转录和翻译方面。 描述的克隆Abelson淋巴瘤系产生主要的B 在培养物中表达Ly-5的220 K同种型的群体，但主要表达Ly-5的220 K同种型。 体内表达200 K同种型的T细胞群。 如果这个概念是正确的 原始转化细胞因此是祖细胞， 淋巴细胞，我们有一个有价值的模型， （T与B），用于研究谱系相关亚型的调节 表情 我们的目标首先是确定替代路线 这些Abelson线采用的实际上符合正常的T和B 在Ly-5转录和翻译方面的谱系。 关于220 K（B-like）Ly-5产物的异常表达， 我们在lpr/lpr的扩增的Ly 1 T细胞群中观察到， gld/gld小鼠淋巴细胞增殖综合征，我们的目的是解决 这个220 K是否与220 K亚型无法区分的问题 正常B细胞或增殖Ly 1细胞特有的产物，无论 增殖是正常还是不正常。 （LB）

Various aspects and models of the regulation of T-cell differentiation are addressed. Evidence is given that certain T-cell lymphoma clones are inducible to express Lyt-1 in vitro. The blocking of Lyt-1 expression and accompanying IL-2 production by Ly-5 monoclonal antibody, and other data, suggest to us that Ly-5 on pre-Lyl cells is involved in the IL-1 dependent step leading to IL-2 production and the Lyl phenotype. We aim to characterize this transition in terms of transcription and translation. We find that recombinant gamma-interferon can induce the Lyb-2 and suceeding sIg surface phenotypes of B lineage cells. A point of special interest is that this requires far less gamma-interferon than is needed in conventional virus-protection (CPE) assay. Gamma-interferon may thus deserve consideration as an agent of lymphocyte differentiation even in circumstances where ordinary CPE assay does not reveal its presence. The meaning of Lyt-1 expression by a sub-set of B cells as well as the Ly1 and Ly123 sets of T cells is obscure. We aim to elucidate the induced augmentation of Lyt-1 we observe in mitogen-stimulated clonal B cells, in terms of transcription and translation in comparison with T cells. The clonal Abelson lymphoma lines described generate a predominant B population expressing the 220K isoform of Ly-5 in culture but a predominant T population expressing the 200K isoform in vivo. If the notion is correct that the originating transformed cell was therefore the progenitor cell for lymphocytes, we have a valuable model of alternative differentional options (T versus B) with which to study the regulation of lineage-related isoform expression. We aim first to determine whether the alternative routes adopted by these Abelson lines in fact conform to the normal T and B lineages in terms of Ly-5 transcription and translation. With regard to the aberrant expression of a 220K (B-like) Ly-5 product which we observe in the expanding Ly1 T cell population of lpr/lpr and gld/gld mice with lympho-proliferative syndrome, we aim to settle the question of whether this 220K is indistinguishable from the 220K isoforms of normal B cells or a product peculiar to proliferating Ly1 cells, whether that proliferation is normal or abnormal. (LB)