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A pivotal role for the multifunctional calcium/calmodulin-dependent protein kinase ii in t cells: From activation to unresponsiveness

Academic Article
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Overview

authors

  • Lin, M. Y.
  • Zal, T.
  • Ch'en, I. L.
  • Gascoigne, Nicholas
  • Hedrick, S. M.

publication date

  • May 2005

journal

  • Journal of Immunology  Journal

abstract

  • 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 CaMKIIbeta, CaMKIIbeta'e, in mouse T cells. We have determined its function, along with that of CaMKIIgamma, 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.

subject areas

  • Alternative Splicing
  • Animals
  • Antigens
  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Cell Proliferation
  • Cell Survival
  • Clonal Anergy
  • Cytokines
  • Cytotoxicity, Immunologic
  • Enzyme Activation
  • Isoenzymes
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Multienzyme Complexes
  • Transduction, Genetic
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 15843557
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Additional Document Info

start page

  • 5583

end page

  • 5592

volume

  • 174

issue

  • 9

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