Roles of CRAC and Cav-like channels in T cells: more than one gatekeeper?

Abstract:

:Ca2+ channels in the plasma membrane of T cells vitally influence Ca2+-dependent signals that lead ultimately to cytokine secretion, cellular proliferation and apoptosis. Conventional models depict the Ca2+ inrush across the T-cell membrane following T-cell receptor engagement as being due to Ca2+-release-activated Ca2+ (CRAC) channels. A poorly understood mechanism detects the lowered Ca2+ concentrations within intracellular stores that open CRAC channels. Mammalian homologs of the Drosophila transient receptor potential Ca2+ channels possibly help to gate the store-operated, Ca2+-borne CRAC current. In this article, we review evidence of a supplementary involvement of other Ca2+ channels, the opening of which does not necessarily reflect intracellular Ca2+-store depletion. We highlight a role for variants of L-type voltage-dependent Ca2+ channels in increasing intracellular Ca2+ concentrations during activation. For more-accurate modeling of lymphocyte activation and possible pharmacological interventions, future research should aim to identify physiologically relevant situations in which such channels help to shape the Ca2+ signal.

journal_name

Trends Pharmacol Sci

authors

Kotturi MF,Hunt SV,Jefferies WA

doi

10.1016/j.tips.2006.05.007

subject

Has Abstract

pub_date

2006-07-01 00:00:00

pages

360-7

issue

7

eissn

0165-6147

issn

1873-3735

pii

S0165-6147(06)00133-7

journal_volume

27

pub_type

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