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STIM1-independent T cell development and effector function in vivo

Niklas Beyersdorf1, Attila Braun, Timo Vögtle

  • 1Institute for Virology and Immunobiology, Deutsche Forschungsgemeinschaft Research Center for Experimental Biomedicine, University of Würzburg, Germany.

Journal of Immunology (Baltimore, Md. : 1950)
|March 7, 2009
PubMed

Insights

Store-operated calcium entry (SOCE) regulated by STIM1 is vital for T cell proliferation. However, STIM1 deficiency did not impede T cell maturation or effector functions in this study.

Area of Science:

  • Immunology
  • Cell Biology
  • Calcium Signaling

Background:

  • Store-operated calcium entry (SOCE) is critical for T cell function.
  • Stromal interaction molecule 1 (STIM1) is a key regulator of SOCE.

Purpose of the Study:

  • To investigate the role of STIM1-dependent SOCE in T cell physiology.
  • To determine the necessity of STIM1 for T cell maturation, proliferation, and effector functions.

Main Methods:

  • Generation of STIM1-deficient mice.
  • In vitro analysis of calcium flux in T cells.
  • In vivo studies including vaccination and adoptive T cell transfer.
  • Generation of bone marrow chimeric mice.

Main Results:

  • STIM1 deficiency abolished SOCE and antigen receptor-triggered calcium flux in T cells.
  • STIM1-deficient mice exhibited lymphoproliferative disease.
  • T cell maturation and regulatory T cell frequencies were normal.
  • Humoral immune responses and graft-versus-host disease induction were intact.

Conclusions:

  • STIM1-dependent SOCE is essential for T cell homeostasis and proliferation.
  • STIM1 is less critical for T cell differentiation and effector functions.
  • SOCE is not required for thymic T cell maturation or immune responses like vaccination.

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