Rudolphi A, Bonhagen K, Reimann J
Institute for Medical Microbiology and Immunology, University of Ulm, Germany.
Eur J Immunol. 1996 May;26(5):1156-63. doi: 10.1002/eji.1830260529.
The adoptive transfer of low numbers of peripheral, non-fractionated CD4+ alpha beta T cells into histocompatible, severely immunodeficient (scid) hosts induces a colitis. This disease developed in C.B-17 scid/scid hosts after the injection of 10(5) CD4+ T cells purified from different peripheral lymphoid organs of immunocompetent C.B.-17 +/+ or BALB/cdm2 donor mice. Irrespective of their tissue origin, transferred CD4+ T cells selectively repopulated the scid host with gut-seeking CD4+ T cells. A chronic inflammatory bowel disease (IBD) developed as polyclonal populations of mucosa-seeking memory/effector CD4+ T cells accumulated in the gut lamina propria and epithelial layer of the adoptive host. The manifestation of colitis in the scid host correlated with the in situ polyclonal activation and expansion of adoptively transferred CD4+ T cells in the colonic lamina propria. Attempts were unsuccessful to select in vivo an oligoclonal CD4+ T cell population with an enhanced IBD-inducing potential by repeatedly reinjecting 10(5) donor-type CD4+ T cells from the colonic lamina propria of transplanted scid mice with an early and severe IBD into new scid hosts. The data indicate that the preferential repopulation of gut-associated lymphoid tissues with immunocompetent CD4+ T cells, and their polyclonal activation and in situ expansion in the lamina propria of the histocompatible, immunodeficient host are critical events in the pathogenesis of an IBD in this model.
将少量外周血未分离的CD4+αβT细胞移植到组织相容性良好、严重免疫缺陷（scid）的宿主中会诱发结肠炎。在向C.B-17 scid/scid宿主注射从免疫活性C.B.-17 +/+或BALB/cdm2供体小鼠不同外周淋巴器官纯化的10(5)个CD4+ T细胞后，这种疾病就会发生。无论其组织来源如何，移植的CD4+ T细胞都会选择性地使scid宿主重新填充肠道归巢的CD4+ T细胞。随着多克隆的黏膜归巢记忆/效应CD4+ T细胞群体在过继宿主的肠道固有层和上皮层中积累，会发展出一种慢性炎症性肠病（IBD）。scid宿主中结肠炎的表现与过继转移的CD4+ T细胞在结肠固有层中的原位多克隆激活和扩增相关。通过反复将患有早期严重IBD的移植scid小鼠结肠固有层中的10(5)个供体型CD4+ T细胞重新注射到新的scid宿主中，试图在体内选择具有增强IBD诱导潜力的寡克隆CD4+ T细胞群体，但未成功。数据表明，免疫活性CD4+ T细胞优先重新填充肠道相关淋巴组织，以及它们在组织相容性免疫缺陷宿主的固有层中的多克隆激活和原位扩增是该模型中IBD发病机制的关键事件。
