Control of the proliferation of activated CD4+ T cells by connexins

Journal of Leukocyte Biology

Ilaria Potolicchio²  W. Howard Evans³  Ernesto Oviedo-Orta¹  Matthieu Perreau² 

[1] Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom; Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom; Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom;;Laboratory of AIDS, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland Laboratory of AIDS, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland Laboratory of AIDS, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland;School of Medicine, Department of Infection, Immunity and Biochemistry, Cardiff University, Wales, United Kingdom; and School of Medicine, Department of Infection, Immunity and Biochemistry, Cardiff University, Wales, United Kingdom; and School of Medicine, Department of Infection, Immunity and Biochemistry, Cardiff University, Wales, United Kingdom; and

关键词: connexin 43;    T cell receptor;    hemichannels;    cysteine uptake;    cell cycle;    lymphocytes;    gap junction;   

DOI  :  10.1189/jlb.0909613

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

As expression of Cxs in cells of the immune system increases upon cellular activation, we investigated whether Cxs and especially CxHcs play a major role during T cell-mediated responses. In particular, we studied the expression of Cx43Hc following CD4+ T cell stimulation using flow cytometry, real-time PCR, and Western blot analysis. We showed that expression of Cx43 and its phosphorylated isoforms increased in response to the engagement of CD3 and CD28. Cx43Hcs were found to be involved in sustaining proliferation of T cells, as assessed by cell cycle staining, thymidine incorporation assays, and CFSE analysis of cells exposed to mimetic peptide inhibitors of the plasma membrane Cx channels and antibodies generated to an extracellular region of Cx. The reduction of T cell proliferation mediated by Cx channel inhibitors suppressed cysteine uptake but not cytokine production. We conclude that upon antigen recognition, T cells require CxHc to sustain their clonal expansion.

【 授权许可】

Unknown