Bregenholt S, Brimnes J, Reimann J, Claesson M H
Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Denmark.
Clin Exp Immunol. 1998 Oct;114(1):19-25. doi: 10.1046/j.1365-2249.1998.00691.x.
Scid mice transplanted either with a gut wall graft or with low numbers of purified CD4+ T cells from immunocompetent syngeneic donor mice show clinical signs of IBD 3-4 months post-transplantation. The disease is mediated by mucosa-infiltrating CD4+ TCR alphabeta+ T cells. The pathology of 52 individual colon segments obtained from 20 gut wall- or CD4+ T cell-transplanted diseased scid mice was evaluated by histology and the numbers of infiltrating immunoglobulin-containing cells were determined. In particular, cells positive for IgM, IgA and non-inflammatory immunoglobulin isotypes such as IgG1 and IgG2b were found to accumulate in colon segments displaying the most severe histopathology, including inflammatory cellular infiltration, epithelial hyperplasia and ulcerative lesions. Compared with colon segments of normal C.B-17 mice, the lesional scid colon shows increased levels of cells positive for the IgG classes. Faecal extracts of the CD4+ T cell-transplanted scid mice revealed the presence of all six murine immunoglobulin isotypes. Disease progression was accompanied by an increased level of excreted IgM and IgG3 and decreased levels of IgA. It is concluded that locally secreted immunoglobulins may play an immunomodulating role in the pathological changes observed in the present model of T cell-induced inflammatory bowel disease.
移植了来自免疫活性同基因供体小鼠的肠壁移植物或少量纯化CD4+ T细胞的重度联合免疫缺陷(Scid)小鼠,在移植后3 - 4个月出现炎症性肠病(IBD)的临床症状。该疾病由浸润黏膜的CD4+ TCR αβ+ T细胞介导。通过组织学评估了从20只接受肠壁或CD4+ T细胞移植的患病Scid小鼠获得的52个单个结肠段的病理情况,并确定了浸润的含免疫球蛋白细胞的数量。特别是,发现IgM、IgA以及非炎性免疫球蛋白同种型(如IgG1和IgG2b)阳性的细胞在显示最严重组织病理学的结肠段中积聚,包括炎性细胞浸润、上皮增生和溃疡性病变。与正常C.B - 17小鼠的结肠段相比,病变的Scid结肠中IgG类阳性细胞水平升高。CD4+ T细胞移植的Scid小鼠的粪便提取物显示存在所有六种小鼠免疫球蛋白同种型。疾病进展伴随着排泄的IgM和IgG3水平升高以及IgA水平降低。得出的结论是,局部分泌的免疫球蛋白可能在目前T细胞诱导的炎症性肠病模型中观察到的病理变化中发挥免疫调节作用。