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Regulation of lymphocyte function by ORAI and STIM proteins in infection and autoimmunity

Patrick J Shaw1, Stefan Feske

  • 1Department of Pathology, New York University Medical Center, 550 First Avenue, SRB 316, New York, NY 10016, USA.

The Journal of Physiology
|May 23, 2012
PubMed

Insights

Store-operated Ca(2+) entry (SOCE) via CRAC channels is crucial for immune cell function. Mutations impairing these channels cause CRAC channelopathy, leading to immunodeficiency and autoimmunity.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Store-operated Ca(2+) entry (SOCE) is essential for immune cell function.
  • CRAC channels, formed by ORAI and STIM proteins, mediate SOCE.
  • Defects in SOCE lead to CRAC channelopathy, a syndrome of immunodeficiency and autoimmunity.

Purpose of the Study:

  • To review the role of CRAC channels in immune cell function.
  • To discuss the impact of CRAC channel defects on adaptive immunity.
  • To explore the implications for autoimmunity and inflammation.

Main Methods:

  • Literature review of studies on CRAC channels, ORAI, and STIM proteins.
  • Analysis of clinical data from patients with CRAC channelopathy.
  • Discussion of lymphocyte subset function in relation to SOCE.

Main Results:

  • Loss-of-function mutations in ORAI1 and STIM1 abolish CRAC channel function and SOCE.
  • Impaired SOCE affects CD8(+) T cells, CD4(+) T cells, NK cells, and B cells.
  • CRAC channelopathy results in severe immunodeficiency and autoimmunity.

Conclusions:

  • CRAC channels are critical regulators of adaptive immune responses.
  • Dysfunctional SOCE underlies CRAC channelopathy, impacting infection immunity and autoimmunity.
  • Targeting CRAC channels may offer therapeutic avenues for immune disorders.

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