Infection of Nippostrongylus brasiliensis induces development of mucosal-type but not connective tissue-type mast cells in genetically mast cell-deficient Ws/Ws rats.
Infection of Nippostrongylus brasiliensis induces development of mucosal-type but not connective tissue-type mast cells in genetically mast cell-deficient Ws/Ws rats.
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DOI：
10.1182/blood.v81.10.2572.bloodjournal81102572
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发表时间：
1993
期刊：
影响因子：
20.3
通讯作者：
Minoru Yamada;Manabu Okada;Masahiro Morimoto;Hideki Tei;G. Newlands;Hugh;P. R.;Miller;Yukihiko Kitamura
中科院分区：
文献类型：
--
作者：
Minoru Yamada;Manabu Okada;Masahiro Morimoto;Hideki Tei;G. Newlands;Hugh;P. R.;Miller;Yukihiko Kitamura
Ws/Ws 大鼠的 c-kit 基因的酪氨酸激酶结构域有一个小缺失，并且粘膜肥大细胞 (MMC) 和结缔组织型肥大细胞 (CTMC) 均缺乏。通过用巴西圆线虫 (NB) 感染 Ws/Ws 和对照 +/+ 大鼠来研究 c-kit 受体在 MMC 和 CTMC 发育中的作用，NB 会诱导 T 细胞依赖性肥大细胞增殖。尽管Ws/Ws大鼠的皮肤中没有出现肥大细胞，但NB感染后空肠中出现了大量的肥大细胞。这些肥大细胞具有 MMC 蛋白酶表型（大鼠肥大细胞蛋白酶 [RMCP] I-/II+），并且缺乏肝素，因为它们未用硫酸小檗碱染色。在这些大鼠的粘膜上皮中也检测到球状白细胞。然而，NB感染的Ws/Ws大鼠中MMC的数量和RMCP II的血清浓度分别仅为NB感染的+/+大鼠的13%和7%。 NB感染后Ws/Ws大鼠的肺、肝、肠系膜淋巴结中也出现少量肥大细胞。尽管这些组织中的肥大细胞在整个观察期间都具有MMC表型，但+/+大鼠肺和肝脏中增加的肥大细胞获得了CTMC样表型，并且具有RMCP I+/II+、硫酸小檗碱+和福尔马林抗性。这些结果表明，皮肤中 CTMC 的发育以及肺和肝脏中 CTMC 样肥大细胞的发育似乎比 MMC 的发育更需要通过 c-kit 受体的刺激。
Ws/Ws rats have a small deletion at the tyrosine kinase domain of the c-kit gene and are deficient in both mucosal mast cells (MMC) and connective tissue-type mast cells (CTMC). The role of the c-kit receptor in the development of MMC and CTMC was investigated by infecting Ws/Ws and control +/+ rats with Nippostrongylus brasiliensis (NB), which induces T-cell-dependent mast cell proliferation. Although mast cells did not develop in the skin of Ws/Ws rats, a significant number of mast cells developed in the jejunum after NB infection. These mast cells had the MMC protease phenotype (rat mast cell protease [RMCP] I-/II+) and lacked heparin because they were not stained with berberine sulfate. Globule leukocytes were also detected in the mucosal epithelium of these rats. However, the number of MMC and the serum concentration of RMCP II in NB-infected Ws/Ws rats were only 13% and 7% of those of NB-infected +/+ rats, respectively. A small number of mast cells also developed in the lung, liver, and mesenteric lymph nodes of Ws/Ws rats after NB infection. Although mast cells in these tissues had the MMC phenotype throughout the observation period, the increased mast cells in the lung and liver of +/+ rats acquired a CTMC-like phenotype and were RMCP I+/II+, berberine sulfate+, and formalin resistant. These results indicate that the need for the stimulus through the c-kit receptor appears to be greater in the development of CTMC in the skin as well as for CTMC-like mast cells in the lung and liver than for the development of MMC.