Befus A D, Bienenstock J
Immunology. 1979 Sep;38(1):95-101.
To investigate mechanisms of mast-cell proliferation, we have utilized infection of Lewis rats with the intestinal nematode, Nippostrongylus brasiliensis, which induces a pronounced intestinal mast-cell hyperplasia. Adoptive transfer of 2 x 10(8) immune mesenteric lymph node cells (IMLN), collected 14 days post infection with 3000 third stage larvae (L3), into rats concurrently given 3000 L3 hastened the expected intestinal mastocytosis by up to 4-5 days. IMLN exhibited this mastopoietic activity in the presence but not in the absence of concurrent infection. Normal mesenteric lymph node cells did not show similar mastopoietic activity. Intestinal mastocytosis was delayed by sub-lethal irradiation (400 rad) but IMLN reconstituted the mast-cell response of such animals. The mastopoietic activity could not be attributed to worm antigen as antigen administered intravenously had no significant effect on mastocytosis and furthermore, antigen could not be detected in mastopoietically active IMLN suspensions used as a possible antigen source in passive cutaneous anaphylaxis tests. Immune serum (14 days post primary infection with 3000 L3) also hastened mastocytosis in infected rats, whereas normal serum did not. The IMLN may be an enriched source of intestinal mast cell precursors and, in addition, may contain a cell type(s) which regulates the differentiation and proliferation of such precursors.
为了研究肥大细胞增殖的机制,我们利用巴西日圆线虫感染Lewis大鼠,该线虫可诱导明显的肠道肥大细胞增生。将感染3000条第三期幼虫(L3)14天后收集的2×10⁸免疫肠系膜淋巴结细胞(IMLN)过继转移到同时接种3000条L3的大鼠体内,可使预期的肠道肥大细胞增多提前4 - 5天出现。IMLN在同时存在感染的情况下表现出这种促肥大细胞生成活性,而在无同时感染时则无此活性。正常肠系膜淋巴结细胞未表现出类似的促肥大细胞生成活性。亚致死剂量照射(400拉德)可延迟肠道肥大细胞增多,但IMLN可重建此类动物的肥大细胞反应。促肥大细胞生成活性不能归因于蠕虫抗原,因为静脉注射抗原对肥大细胞增多无显著影响,此外,在被动皮肤过敏试验中用作可能抗原来源的具有促肥大细胞生成活性的IMLN悬液中未检测到抗原。免疫血清(初次感染3000条L3后14天)也可加速感染大鼠的肥大细胞增多,而正常血清则无此作用。IMLN可能是肠道肥大细胞前体的丰富来源,此外,可能含有一种或多种调节此类前体分化和增殖的细胞类型。