Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 9, Pages 5794-5798Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.9.5794
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Funding
- NCI NIH HHS [T32 CA101968, R01 CA105216, R01 CA105216-02, CA 101968, R01 CA 105216] Funding Source: Medline
- NIAID NIH HHS [R01 AI057838-02, R01 AI057838-01A1, R01 AI 057838, R01 AI057838-05, R01 AI057838-03, R01 AI057838, R01 AI057838-04] Funding Source: Medline
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Addition of rapamycin to cultures of expanding natural If CD4(+)CD25(+)Foxp3(+) T regulatory cells (Tregs) helps maintain their suppressive activity, but the underlying mechanism is unclear. Pim 2 is a serine/threonine kinase that can confer rapamycin resistance. Unexectedly, pim 2 was found to be constitutively expressed in freshly isolated, resting Tregs, but not in CD4(+) CD25(-) T effector T cells induced pim 2 expression and conferred preferential expansion in the presence of rapamycin, indicating that Foxp3 can regulate pim 2 expression. Finally, we determined there is a positive correlation between Treg expansion and Toxp3 expression in the presence of rapamycin. Together, these results indicate that Tregs are programmed to be resistant to rapamycin, providing further rationale for why this immunosuppressive drug should be used in conjunction with expanded Tregs.
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