Synergy between intraepithelial lymphocytes and lamina propria T cells drives intestinal inflammation during infection.
Synergy between intraepithelial lymphocytes and lamina propria T cells drives intestinal inflammation during infection.
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作者：
C57 BL/6小鼠经口感染弓形虫在感染后7-10天内引起回肠严重坏死。病变发展由Th-1细胞因子、CD 4 + T细胞和上皮下细菌移位介导。因此，这些特征与克罗恩病具有相似性。最近，我们发现了上皮内淋巴细胞（IEL）介导的弓形虫感染后的病理作用。我们发现αβ而不是γδ T细胞IEL介导肠道损伤。通过将粘膜T细胞过继转移到幼稚Rag 1 −/−小鼠中，我们证明IEL不单独起作用以引起炎性病变，而是与来自固有层的CD 4 + T淋巴细胞一起起作用。此外，用广谱抗生素预处理以消除肠道植物群的受体小鼠在转移IEL和固有层淋巴细胞后抵抗肠道疾病。我们的数据为肠道炎症机制提供了有价值的新见解，这些发现对理解人类炎症性肠病具有重要意义。
Oral infection of C57BL/6 mice with Toxoplasma gondii triggers severe necrosis in the ileum within 7–10 days of infection. Lesion development is mediated by Th-1 cytokines, CD4+ T cells, and sub-epithelial bacterial translocation. As such, these features share similarity to Crohn’s disease. Recently, we uncovered a role for intraepithelial lymphocytes (IEL) in mediating pathology after Toxoplasma infection. We show here that αβ and not γδ T cell IELs mediate intestinal damage. By adoptive transfer of mucosal T cells into naive Rag1−/− mice, we demonstrate that IEL do not function alone to cause inflammatory lesions, but act with CD4+ T lymphocytes from the lamina propria. Furthermore, recipient mice pretreated with broad-spectrum antibiotics to eliminate intestinal flora resisted intestinal disease after transfer of IEL and lamina propria lymphocytes. Our data provide valuable new insight into mechanisms of intestinal inflammation, findings that have important implications for understanding human inflammatory bowel disease.
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影响因子：
30.3
作者：
Benson A;Pifer R;Behrendt CL;Hooper LV;Yarovinsky F
通讯作者：
Yarovinsky F
DOI：
10.1084/jem.20020258
发表时间：
2002-06-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Barragan A;Sibley LD
通讯作者：
Sibley LD
影响因子：
15.3
作者：
El-Asady, R;Yuan, RW;Hadley, GA
通讯作者：
Hadley, GA
影响因子：
6.4
作者：
Liesenfeld, O
通讯作者：
Liesenfeld, O
影响因子：
2.2
作者：
Liesenfeld, O;Kang, H;Suzuki, Y
通讯作者：
Suzuki, Y