4.6 Review

Galectin-3 modulation of T-cell activation: mechanisms of membrane remodelling

Journal

PROGRESS IN LIPID RESEARCH
Volume 76, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.plipres.2019.101010

Keywords

Galectin-3; Glycolipids; T cell activation; Immunological synapse; T cell signalling; Immunotherapy

Funding

  1. Australian Research Council (ARC) [CE140100011]
  2. National Health and Medical Research Council of Australia [APP1155162]
  3. NSW Cancer Council [APP1128488]
  4. European Research Council [340485]
  5. European Research Council (ERC) [340485] Funding Source: European Research Council (ERC)

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Galectin-3 (Gal3) is a multifaceted protein which belongs to a family of lectins and binds beta-galactosides. Gal3 expression is altered in many types of cancer, with increased expression generally associated with poor prognosis. Although the mechanisms remain unknown, Gal3 has been implicated in several biological processes involved in cancer progression, including suppression of T cell-mediated immune responses. Extracellular Gal3 binding to the plasma membrane of T cells alters membrane organization and the formation of an immunological synapse. Its multivalent capacity allows Gal3 to interact specifically with different membrane proteins and lipids, influencing endocytosis, trafficking and T cell receptor signalling. The ability of Gal3 to inhibit T cell responses may provide a mechanism by which Gal3 aids in cancer progression. In this review, we seek to give an overview of the mechanisms by which Gal3 alters the spatial organization of cell membranes and how these processes impact on T cell activation.

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