Gut mucosal mast cells. Origin, traffic, and differentiation.
Gut mucosal mast cells. Origin, traffic, and differentiation.
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DOI：
10.1084/jem.160.1.12
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发表时间：
1984-07-01
期刊：
影响因子：
--
通讯作者：
Vassalli P
中科院分区：
文献类型：
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作者：
Guy-Grand D;Dy M;Luffau G;Vassalli P
肠道粘膜肥大细胞（MMC），这是几乎没有在正常小鼠是丰富的线虫感染期间。在正常小鼠中，MMC前体的研究（MMC-P：在IL-3存在下产生MMC集落的细胞）显示：（a）通过有限稀释判断，它们的频率在骨髓（BM）和肠中非常高，而在大多数淋巴器官和胸导管淋巴（TDL）中非常低;（B）肠MMC-P是Thy-1- Lyt-1-2-，并且不快速复制;（c）它们是分化程度较低的BM MMC-P的后代，其通过局部因子而不是抗原和T细胞因子从血液吸引到肠粘膜（因为在无菌、裸鼠和新生小鼠中发现了正常量的肠MMC-P）。在携带Wehi 3肿瘤的小鼠中，（其释放足够的IL-3以产生可检测的血液水平）脾和肠系膜淋巴结（LN）显示MMC-P频率增加，最大的增加是在肠道和BM中，其中发现许多分化的MMC。（已知产生大的T细胞依赖性的肠MMC浸润），肠MMC-P增殖由肠粘膜Thy-1+ Lyt-2-细胞释放的IL-3诱导，其体外释放IL-3的能力远高于正常小鼠的同类细胞。Nb刺激的T胚细胞和增殖的MMC-P都经历循环运输，迁移到TDL中，然后接种肠道的整个长度（在局部抗原刺激后允许广泛的免疫防御的过程）。使用2-d中断这种交通和胎儿肠道移植物的实验表明，T母细胞持续归巢回到肠道，导致永久性Nb刺激的IL-3释放，是MMC完全成熟所必需的。在大鼠中的转移实验表明，TDL循环MMC-P迅速成熟为MMC时，他们回家到Nb感染的肠道。提示肠道MMC在MMC-P进行性分化的几个阶段后出现，受IL-3和未鉴定的肠道因子的影响。
Gut mucosal mast cells (MMC), which are nearly absent in normal mice are abundant during nematode infection. In normal mice, study of MMC precursors (MMC-P: cells giving rise to MMC colonies in the presence of IL-3) show that: (a) their frequency, judged by limiting dilution is very high in bone marrow (BM) and gut, and very low in most lymphoid organs and thoracic duct lymph (TDL); (b) gut MMC-P are Thy-1- Lyt-1-2- and are not rapidly replicating; (c) they are the progeny of less differentiated BM MMC-P which are attracted from the blood to the gut mucosa by local factor(s), other than antigen and T cell factors (since normal amounts of gut MMC-P are found in germ-free, nude, and newborn mice). In mice bearing the Wehi 3 tumor (which releases enough IL-3 to produce detectable blood levels) spleen and mesenteric lymph nodes (LN) show increased MMC-P frequency, the greatest increase being in the gut and BM, where numerous differentiated MMC are found. In Nippostrongylus brasiliensis (Nb)-infested mice (known to develop a large, T cell- dependent, gut MMC infiltration), gut MMC-P proliferation is induced by IL-3 released from gut mucosal Thy-1+ Lyt-2- cells, whose in vitro IL-3 release capability is much higher than that of similar cells from normal mice. Both Nb-stimulated T blasts and proliferating MMC-P undergo cyclic traffic, migrating into the TDL and then seeding the whole length of the gut (a process which allows a widespread immune defense after a local antigenic stimulus). Experiments using 2-d interruption of this traffic and fetal gut grafts, suggest that the continuous homing of T blasts back to the gut which leads to permanent Nb-stimulated IL-3 release, is essential for the full maturation of MMC. Transfer experiments in the rat show that TDL circulating MMC-P rapidly mature into MMC when they home back to the Nb-infested gut. It is proposed that gut MMC arise after several stages of progressive differentiation of MMC-P, influenced both by IL-3 and unidentified gut factor(s).