T CELL DEVELOPMENT: IMMUNOGENETICS, DEFECTS, THERAPY

三个新表征的调节分子正在研究中， 比较它们在体内诱导(单独或联合) 人外周血中表型和功能成熟T细胞的分化 无菌幼年NU/NU小鼠(不到三个月龄)。它们包括： (1)新合成的抗蛋白酶TP-5类似物(对应于 胸腺生成素残基32-36)；(2)类似地衍生的脾五肽， 它与TP-5不同，只有一个氨基酸取代，但诱导 T和B细胞在体外的表型分化； 重组干扰素-γ，发现可诱导T细胞和B细胞 体外分化。 两种突变小鼠新的表型和功能比较研究 分别携带未连接的GLD和LPR基因的菌株，这些基因会导致 类似的全身性淋巴增生性疾病和自身免疫综合征 应指示非等位基因突变体的正常对应物是否 基因LPR和GLD通过相同的调控机制发挥作用，即 在LPR和GLD纯合子小鼠中受影响。(磅)

Three newly characterized regulatory molecules are being studied and compared for their activity in vivo to induce (alone or in combination) the differentiation of phenotypically and functionally mature T cells in germ-free young nu/nu mice (less than three months of age). They include: (1)\a newly synthesized protease resistant TP-5 analog (corresponding to thymopoietin residues 32-36); (2) a similarly derived splenic pentapeptide, which differs from TP-5 by one amino acid substitution, but induces the phenotypic differentiation of both T and B cells in vitro; and (3) recombinant interferon-gamma, found to induce both T-\and B-cell differentiation in vitro. New comparative phenotypic and functional studies of two mutant mouse strains carrying, respectively, the unlinked gld and lpr genes that cause a similar generalized lymphoproliferative disorder and autoimmune syndrome should indicate whether the normal counterparts of the nonallelic mutant genes lpr and gld function through the same regulatory mechanism that is affected in lpr and gld homozygous mice. (LB)