Open Access
Article
Deregulation of calcium fluxes in HTLV-I infected CD4-positive T-cells plays a major role in malignant transformation
Haidar Akl1,Bassam Badran1,Nabil El Zein1,Gratiela Dobirta1,Arsene Burny1,Philippe Martiat1
1
Experimental Hematology, Universite Libre de Bruxelles, Institut Jules Bordet 127 Boulevard de Waterloo, 1000 Bruxelles, Belgium. haidar.akl@ulb.ac.be
DOI: 10.2741/3501 Volume 14 Issue 10, pp.3925-3934
Published: 01 January 2009
Abstract

The CD4+ T-cell malignancy induced by human T-cell leukemia virus type 1 (HTLV-I) infection and termed; Adult T-cell Leukemia lymphoma (ATLL), is caused by defects in the mechanisms underlying cell proliferation and cell death. In the CD4+ T-cells, calcium ions are central for both phenomena. ATLL is associated with a marked hypercalcemia in many patients. The consequence of a defect in the Ca2+ signaling pathway for lymphocyte activation is characterized by an impaired NFAT activation and transcription of cytokines, chemokines and many other NFAT target genes whose transcription is essential for productive immune defense. Fresh ATLL cells lack the TCR/CD3 and CD7 molecules on their surface. Whereas CD7 is a calcium transporter, reduction in calcium influx in response to T-cell activation was reported as a functional consequence of TCR/CD3 expression deficiency. Understanding these changes and identifying the molecular players involved might provide further insights on how to improve ATLL treatment.

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Haidar Akl, Bassam Badran, Nabil El Zein, Gratiela Dobirta, Arsene Burny, Philippe Martiat. Deregulation of calcium fluxes in HTLV-I infected CD4-positive T-cells plays a major role in malignant transformation. Frontiers in Bioscience-Landmark. 2009. 14(10); 3925-3934.