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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Distinct pathways involving the FK506-binding proteins 12 and 12.6 underlie IL-2-versus IL-15-mediated proliferation of T cells.
The molecular basis for the different roles of IL-2 and IL-15 in lymphocyte function has been poorly defined. Searching for differences that underlie the distinct T cell responses to the two cytokines, we observed a marked susceptibility of the IL-15- induced but not of the IL-2- induced proliferation to rapamycin despite a decrease of p70S6 kinase (p70S6K) activation by the drug in response to both cytokines. Activated splenic T lymphocytes deficient in the FK506-binding protein (FKBP) 12, a target of rapamycin activity, had reduced proliferation in response to IL-15 but not to IL-2. This decreased proliferation was accompanied by reduced activation of p70S6K and of the extracellular signal- regulated kinases ( ERK) after IL-15 treatment. In contrast to FKBP12-/- cells, splenic FKBP12.6-/- T cells exhibited a decreased proliferative response to IL-2 in the presence of rapamycin without affecting p70S6K or ERK activation. Thus, IL-15 induces T cell proliferation mainly via FKBP12- mediated p70S6K activation. In contrast, IL-2 signaling involves multiple pathways that include at least one additional pathway that depends on FKBP12.6.[1]
