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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Barda-saad, Mira Joseph, Noah Reicher, Barak |
| Description | Author Affiliation: Joseph N ( The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 5290002, Israel.); Reicher B ( The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 5290002, Israel.); Barda-Saad M ( The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 5290002, Israel. Electronic address: Mira.Barda-Saad@biu.ac.il.) |
| Abstract | During T cell activation, the engagement of a T cell with an antigen-presenting cell (APC) results in rapid cytoskeletal rearrangements and a dramatic increase of intracellular calcium $(Ca^{2 +})$ concentration, downstream to T cell antigen receptor (TCR) ligation. These events facilitate the organization of an immunological synapse (IS), which supports the redistribution of receptors, signaling molecules and organelles towards the T cell–APC interface to induce downstream signaling events, ultimately supporting T cell effector functions. Thus, $Ca^{2 +}$ signaling and cytoskeleton rearrangements are essential for T cell activation and T cell-dependent immune response. Rapid release of $Ca^{2 +}$ from intracellular stores, e.g. the endoplasmic reticulum (ER), triggers the opening of $Ca^{2 +}$ release-activated $Ca^{2 +}$ (CRAC) channels, residing in the plasma membrane. These channels facilitate a sustained influx of extracellular $Ca^{2 +}$ across the plasma membrane in a process termed store-operated $Ca^{2 +}$ entry (SOCE). Because CRAC channels are themselves inhibited by $Ca^{2 +}$ ions, additional factors are suggested to enable the sustained $Ca^{2 +}$ influx required for T cell function. Among these factors, we focus here on the contribution of the actin and microtubule cytoskeleton. The TCR-mediated increase in intracellular $Ca^{2 +}$ evokes a rapid cytoskeleton-dependent polarization, which involves actin cytoskeleton rearrangements and microtubule-organizing center (MTOC) reorientation. Here, we review the molecular mechanisms of $Ca^{2 +}$ flux and cytoskeletal rearrangements, and further describe the way by which the cytoskeletal networks feedback to $Ca^{2 +}$ signaling by controlling the spatial and temporal distribution of $Ca^{2 +}$ sources and sinks, modulating TCR-dependent $Ca^{2 +}$ signals, which are required for an appropriate T cell response. This article is part of a Special Issue entitled: Reciprocal influences between cell cytoskeleton and membrane channels, receptors and transporters. Guest Editor: Jean Claude Hervé. |
| ISSN | 00063002 |
| Journal | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer |
| Issue Number | 2 |
| Volume Number | 1838 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-02-01 |
| Publisher Place | Netherlands |
| Access Restriction | Open |
| Subject Keyword | Calcium Signaling Calcium Metabolism Cytoskeleton Lymphocyte Activation T-Lymphocytes Animals Signal Transduction Research Support, Non-U.S. Gov't Biochemistry |
| Content Type | Text |
| Resource Type | Article |
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