Journal
JOURNAL OF IMMUNOLOGY
Volume 174, Issue 9, Pages 5583-5592Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.9.5583
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Funding
- NIAID NIH HHS [R01 AI21372-21] Funding Source: Medline
- NIGMS NIH HHS [R01 GM065230] Funding Source: Medline
- NIMH NIH HHS [P30 MH62261] Funding Source: Medline
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Stimulation of the TCR leads to an oscillatory release of free calcium that activates members of the calcium/calmodulin-dependent protein kinase II (CaMKII) family. The CaMKII molecules have profound and lasting effects on cellular signaling in several cell types, yet the role of CaMKII in T cells is still poorly characterized. In this report we describe a splice variant of CaMKII beta, CaMKII beta'e, in mouse T cells. We have determined its function, along with that of CaMKII gamma, by introducing the active and kinase-dead mutants into activated P14 TCR transgenic T cells using retroviral transduction. Active CaMKII enhanced the proliferation and cytotoxic activity of T cells while reducing their IL-2 production. Furthermore, it induced a profound state of unresponsiveness that could be overcome only by prolonged culture in IL-2. These results indicate that members of the CaMKII family play an important role in regulation of CD8 T cell proliferation, cytotoxic effector function, and the response to restimulation.
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