首页> 外文期刊>International immunology. >BALB/c.CBA/N mice carrying the defective Btk(xid) gene are resistant to pristane-induced plasmacytomagenesis.
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BALB/c.CBA/N mice carrying the defective Btk(xid) gene are resistant to pristane-induced plasmacytomagenesis.

机译:携带有缺陷的Btk(xid)基因的BALB / c.CBA / N小鼠对p烷诱导的浆细胞生成具有抗性。

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The X-chromosome from the CBA/N mouse which carries the defective Bruton's tyrosine kinase (Btk) allele (Xxid) has been introgressively backcrossed onto the plasmacytoma (PCT) induction-susceptible BALB/cAN. Inbred BALB/c.CBA/N-xid/xid (C.CBA/N) mice raised and maintained in our conventional colony were given three 0.5 ml injections of pristane and were highly refractory to PCT induction. Only one PCT was found among 59 mice followed for > or =300 days. Twenty mice were examined at day 200 for foci of plasma cells in the oil granuloma. Ten mice had small foci of plasma cells, most of which were plasmacytotic, embedded in the inflammatory oil granuloma. In one there were multiple foci, but most of the mice had only one or two foci. F1 hybrid XxidY males derived from CBA/N females crossed to BALB/cAnPt were also resistant to PCT induction, while heterozygous and homozygous XY males were susceptible. C.CBA/N mice can develop extensive mucosal plasma cells as well as plasma cell accumulations in oil granuloma tissue, but the precursors of these plasma cells do not give rise to PCT in genetically susceptible hosts. The failure of C.CBA/N mice to develop PCT is probably due to the elimination of B cell clones that can be perpetuated by repeated exposure to thymus-independent type 2 antigens.
机译:来自CBA / N小鼠的X染色体携带有缺陷的布鲁顿酪氨酸激酶(Btk)等位基因(Xxid),已进行过质交回与浆细胞瘤(PCT)诱导敏感的BALB / cAN。在我们的常规殖民地饲养和饲养的近交BALB / c.CBA / N-xid / xid(C.CBA/N)小鼠进行了三次0.5 ml的rist烷注射,对PCT的诱导高度耐药。在随后≥300天或= 300天的59只小鼠中,仅发现一种PCT。在第200天检查了20只小鼠的油性肉芽肿中浆细胞的病灶。十只小鼠的浆细胞灶较小,其中大多数是浆细胞性的,包埋在炎性油肉芽肿中。在一个中,有多个病灶,但是大多数小鼠只有一个或两个病灶。来自CBA / N雌性与BALB / cAnPt杂交的F1杂种XxidY雄性也对PCT诱导具有抗性,而杂合和纯合XY雄性易感。 C.CBA/N小鼠可以在油性肉芽肿组织中形成广泛的粘膜浆细胞以及浆细胞积聚,但是这些浆细胞的前体在遗传易感宿主中不会产生PCT。 C.CBA/N小鼠无法发展PCT可能是由于消除了B细胞克隆,这种克隆可以通过反复暴露于不依赖胸腺的2型抗原而得以延续。

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