Calcium signalling in lymphocyte activation and disease

Nat Rev Immunol. 2007 Sep;7(9):690-702. doi: 10.1038/nri2152. Epub 2007 Aug 17.

Abstract

Calcium signals in cells of the immune system participate in the regulation of cell differentiation, gene transcription and effector functions. An increase in intracellular levels of calcium ions (Ca2+) results from the engagement of immunoreceptors, such as the T-cell receptor, B-cell receptor and Fc receptors, as well as chemokine and co-stimulatory receptors. The major pathway that induces an increase in intracellular Ca2+ levels in lymphocytes is through store-operated calcium entry (SOCE) and calcium-release-activated calcium (CRAC) channels. This Review focuses on the role of Ca2+ signals in lymphocyte functions, the signalling pathways leading to Ca2+ influx, the function of the recently discovered regulators of Ca2+ influx (STIM and ORAI), and the relationship between Ca2+ signals and diseases of the immune system.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmunity
  • Calcium / metabolism*
  • Calcium Channels / metabolism
  • Calcium Signaling / immunology*
  • Humans
  • Lymphocyte Activation
  • Lymphocytes / immunology*
  • Membrane Proteins / metabolism
  • Neoplasm Proteins / metabolism
  • ORAI1 Protein
  • Severe Combined Immunodeficiency / immunology*
  • Stromal Interaction Molecule 1

Substances

  • Calcium Channels
  • Membrane Proteins
  • Neoplasm Proteins
  • ORAI1 Protein
  • ORAI1 protein, human
  • STIM1 protein, human
  • Stromal Interaction Molecule 1
  • Calcium