| Autor: |
Boone, David L., Dassopoulos, Themistocles, Chai, Sophia, Chien, Marcia, Lodolce, James, Ma, Averil |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Gastrointestinal & Liver Physiology; Aug2003, Vol. 285 Issue 2, pG382, 7p, 2 Black and White Photographs, 2 Charts, 13 Graphs |
| Abstrakt: |
IL-2 receptor α-deficient (IL2Rα[sup -/-]) mice spontaneously accumulate vast numbers of intestinal lamina propria (LP) T cells and develop bowel inflammation. The accumulation of T cells in IL2Rα[sup -/-] 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 IL2Rα[sup -/-] mice, we have directly examined the proliferation and Fas sensitivity of wild-type, lpr/lpr, and IL2Rα[sup -/-] LP T cells. In wild-type mice, 5'-bromodeoxyuridine (BrdU) labeling and Fas susceptibility are greatest in CD44[sup Hi] LP T cells. Fas-deficient lpr/lpr mice have normal total numbers of LP T cells, despite an increased proportion of BrdU[sup +] T cells. By contrast, IL2Rα[sup -/-] mice possess increased total numbers of LP T cells, despite normal proportions of BrdU[sup +] LP T cells. Finally, wild-type and IL2Rα[sup -/-] LP T cells are equivalently Fas sensitive. These results demonstrate that LP T cells proliferate and are Fas-sensitive cells. IL2Rα[sup -/-] 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 IL2Rα[sup -/-] mice is independent of defective Fas-induced cell death. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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