T-CELL DIFFERENTIATION: MOLECULAR MECHANISMS

T细胞分化调控的各个方面和模型如下 地址。 有证据表明，某些T细胞淋巴瘤克隆可诱导 体外表达Lyt-1。Lyt-1基因表达的阻断及其伴随 Ly-5单抗产生IL-2，以及其他数据向我们暗示 Pre-Lyl细胞上的Ly-5参与了IL-1依赖的阶梯引导 对IL-2的产生和Lyl表型的影响。我们的目标是描述这一点 在转录和翻译方面的过渡。 我们发现重组γ-干扰素可以诱导LYB-2和 获得B系细胞的Sig表面表型。一个特殊的点 有趣的是，这需要的伽马干扰素远远少于 常规病毒保护(CPE)试验。因此，伽马干扰素可以 值得考虑作为淋巴细胞分化剂，即使在 普通CPE化验不能显示其存在的情况。 B细胞亚群和Ly1细胞表达Lyt-1的意义 而Ly123组T细胞则鲜为人知。我们的目标是阐明诱导的 我们在有丝分裂原刺激的克隆性B细胞中观察到Lyt-1的增强 转录和翻译术语与T细胞的比较。 所描述的克隆性Abelson淋巴瘤株产生一个主要的B 在培养中表达Ly-5 220K亚型但占主导地位的群体 体内表达200K亚型的T群体。如果这个概念是正确的 因此，原始的转化细胞是 淋巴细胞，我们有一个有价值的模型，可以选择不同的选择 (T与B)，用于研究谱系相关异构体的调节 表情。我们的目标首先是确定替代路线是否 所采用的这些Abelson线路实际上符合正常的T和B Ly-5转录和翻译方面的谱系。 关于220K(类B)Ly-5产物的异常表达 我们在LPR/LPR和LPR不断扩大的Ly1 T细胞群中观察到 GLD/GLD小鼠淋巴增殖综合征，我们的目标是解决 这个220K与220K异构体是否无法区分的问题 正常B细胞或Ly1细胞特有的增殖产物，无论是 这种增殖是正常的还是不正常的。(磅)

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)