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PMID:12702495

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Citation

Boone, DL, Dassopoulos, T, Chai, S, Chien, M, Lodolce, J and Ma, A (2003) Fas is not essential for lamina propria T lymphocyte homeostasis. Am. J. Physiol. Gastrointest. Liver Physiol. 285:G382-8

Abstract

IL-2 receptor alpha-deficient (IL2Ralpha-/-) mice spontaneously accumulate vast numbers of intestinal lamina propria (LP) T cells and develop bowel inflammation. The accumulation of T cells in IL2Ralpha-/- mice is thought to result, in part, from defective Fas-induced cell death. To understand the role of cell proliferation and death in regulating LP T cells in IL2Ralpha-/- mice, we have directly examined the proliferation and Fas sensitivity of wild-type, lpr/lpr, and IL2Ralpha-/- LP T cells. In wild-type mice, 5'-bromodeoxyuridine (BrdU) labeling and Fas susceptibility are greatest in CD44Hi LP T cells. Fas-deficient lpr/lpr mice have normal total numbers of LP T cells, despite an increased proportion of BrdU+ T cells. By contrast, IL2Ralpha-/- mice possess increased total numbers of LP T cells, despite normal proportions of BrdU+ LP T cells. Finally, wild-type and IL2Ralpha-/- LP T cells are equivalently Fas sensitive. These results demonstrate that LP T cells proliferate and are Fas-sensitive cells. IL2Ralpha-/- mice accumulate a large number of these Fas-sensitive LP T cells and clearly differ from Fas-deficient lpr/lpr mice in this regard. Thus our studies reveal that Fas is dispensable for LP T cell homeostasis and suggest that the intestinal inflammation observed in IL2Ralpha-/- mice is independent of defective Fas-induced cell death.

Links

PubMed Online version:10.1152/ajpgi.00373.2002

Keywords

Animals; Antigens, CD44/analysis; Antigens, CD95/genetics; Antigens, CD95/physiology; Apoptosis; Bromodeoxyuridine/metabolism; Cell Division; Homeostasis; Hypertrophy; Inflammatory Bowel Diseases/etiology; Inflammatory Bowel Diseases/pathology; Intestinal Mucosa/pathology; Intestines/pathology; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Interleukin-2/deficiency; Receptors, Interleukin-2/physiology; T-Lymphocytes/immunology; T-Lymphocytes/pathology; T-Lymphocytes/physiology; Thymectomy

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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