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Publication : An interleukin-7 internet for intestinal intraepithelial T cell development: knockout of ligand or receptor reveal differences in the immunodeficient state.

First Author  Fujihashi K Year  1997
Journal  Eur J Immunol Volume  27
Issue  9 Pages  2133-8
PubMed ID  9341750 Mgi Jnum  J:43129
Mgi Id  MGI:1097184 Doi  10.1002/eji.1830270903
Citation  Fujihashi K, et al. (1997) An interleukin-7 internet for intestinal intraepithelial T cell development: knockout of ligand or receptor reveal differences in the immunodeficient state. Eur J Immunol 27(9):2133-8
abstractText  Both interleukin-7 (IL-7) and IL-7 receptor (R) gene knockout (IL-7-/- and IL-7R-/-) mice were employed in order to directly investigate the importance of the IL-7 and IL-7R signaling pathway for the development of intestinal intraepithelial lymphocytes (IEL). Loss of the IL-7R-specific gene resulted in complete deficiency of the gamma delta T cell lineage with lack of V gamma 4- and V gamma 7-specific messages in the epithelium of the gastrointestinal (GI) tract in comparison to control mice of the same genetic background (approximately 40%). Disruption of the IL-7-specific gene resulted in marked, but not complete depletion of gamma delta T cells (2-3%) in IEL. Furthermore, mRNA for both V gamma 4 and V gamma 7 genes were detected in the gamma delta IEL subset of IL-7-/- mice. The subtle differences between IL-7-/- and IL-7R-/- mice suggest that although IL-7 controls most of the expansion and/or development of gamma delta IEL, another ligand binding to the IL-7R also plays a discernable role. Furthermore, alpha beta IEL developed more slowly in IL-7R-/- mice when compared with ligand knockouts; however, the frequency of IEL T cells subsequently increased with age and normal levels of CD3+ T cells expressing the alpha beta TCR were detected by 2 and 3 months of age in IL-7-/- and IL-7R-/- mice, respectively. The direct comparison of IL-7-/- and IL-7R-/- mice clearly supports the hypothesis that both IL-7 and another IL-7R binding molecule can influence the development of gamma delta T cells in the intestinal epithelium.
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