| First Author | von Freeden-Jeffry U | Year | 1998 |
| Journal | J Immunol | Volume | 161 |
| Issue | 10 | Pages | 5673-80 |
| PubMed ID | 9820548 | Mgi Jnum | J:50984 |
| Mgi Id | MGI:1313154 | Doi | 10.4049/jimmunol.161.10.5673 |
| Citation | von Freeden-Jeffry U, et al. (1998) IL-7 deficiency prevents development of a non-T cell non-B cell- mediated colitis. J Immunol 161(10):5673-80 |
| abstractText | IL-7 is a stromal cell-derived cytokine with a well-established physiologic role in lymphocyte biology. This report describes an unexpected role for IL-7 in the development of colitis in a T and B cell-deficient environment. Recombination-activating gene-2 (RAG-2)- deficient mice (RAG-2(-/-)) were exposed to and subsequently maintained a horizontally transmitted microbial flora that included Helicobacter hepaticus. These animals mounted a strong myeloid cell response and developed both systemic and local signs of a severe colitis. A striking infiltration of F4/80 and MHC class II-positive cells was seen in the colon and cecum of animals undergoing the disease. Mice mutant for both IL-7 and RAG-2 (IL-7/RAG-2(-/-)) that were colonized by the same flora showed no signs of myeloid responses or colitis, indicating that IL-7 plays a critical role in exacerbating a non-T cell/non-B cell-mediated chronic inflammatory response. Recombinant IL-10 protein therapy was able to prevent the occurrence of colitis in susceptible mice, suggesting a pivotal role for macrophages. The implications of a role for IL-7 in this disease model with respect to human inflammatory bowel disease are discussed. |
