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来自巴西日圆线虫感染小鼠的肠系膜淋巴结细胞以及这些细胞在响应3T3成纤维细胞条件培养基时形成的肥大细胞集落中c-kit的表达。

Expression of c-kit by mesenteric lymph node cells from Nippostrongylus brasiliensis-infected mice and by mast cell colonies developing from these cells in response to 3T3 fibroblast-conditioned medium.

作者信息

Leftwich J A, Westin E H, Huff T F

机构信息

Department of Microbiology and Immunology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond 23298.

出版信息

J Immunol. 1992 May 1;148(9):2894-8.

PMID:1374104
Abstract

Mast cell committed progenitors are nongranulated cells found in mesenteric lymph nodes of mice infected with Nippostrongylus brasiliensis (Nb-MLN) but not from normal mice. Mast cell committed progenitors can respond to either IL-3 or to a factor(s) present in 3T3 fibroblast conditioned media (F-CM) by formation of mast cell colonies. Previous studies from ours and other laboratories suggested that mast cell differentiation involved the W allele product, c-kit, as a receptor and Sl allele product, stem cell factor, as a growth factor. We report here that Nb-MLN cells, which can respond to F-CM by mast cell colony formation, also contain cells that express message for c-kit, and that c-kit message cannot be detected in naive mesenteric lymph node cells, which cannot respond to F-CM. Antisense oligonucleotides to c-kit inhibit mast cell colony formation by Nb-MLN cells in response to F-CM, but not to conditioned medium of PWM-stimulated spleen cells as a source of IL-3. The antisense oligonucleotides also inhibit the degree of granulation by mast cells derived from culture. The results suggest that c-kit and its ligand, stem cell factor, are necessary for mast cell-committed progenitors to proliferate and granulate in response to F-CM but not IL-3.

摘要

肥大细胞定向祖细胞是在感染巴西日圆线虫的小鼠肠系膜淋巴结(Nb-MLN)中发现的无颗粒细胞,而正常小鼠中则没有。肥大细胞定向祖细胞可通过形成肥大细胞集落对IL-3或3T3成纤维细胞条件培养基(F-CM)中存在的一种或多种因子作出反应。我们实验室和其他实验室之前的研究表明,肥大细胞分化涉及W等位基因产物c-kit作为受体以及Sl等位基因产物干细胞因子作为生长因子。我们在此报告,能够通过肥大细胞集落形成对F-CM作出反应的Nb-MLN细胞也包含表达c-kit信使的细胞,而在不能对F-CM作出反应的幼稚肠系膜淋巴结细胞中检测不到c-kit信使。针对c-kit的反义寡核苷酸可抑制Nb-MLN细胞对F-CM作出反应而形成肥大细胞集落,但不能抑制作为IL-3来源的PWM刺激的脾细胞条件培养基所诱导的肥大细胞集落形成。反义寡核苷酸还可抑制培养来源的肥大细胞的颗粒化程度。结果表明,c-kit及其配体干细胞因子对于肥大细胞定向祖细胞响应F-CM而非IL-3进行增殖和颗粒化是必需的。

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