Regulation of Human Cytotoxic T Lymphocytes Development by the Synergistic Effect of IL-7 and sCD23 |
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| Institution: | 1. Department of Medicine, Harvard Medical School, Boston, Massachusetts, 02115;3. Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts, 02115;2. Ospedale Civile di Latina, Latina, Italy;1. Leicester Cancer Research Centre, University of Leicester, Leicester Royal Infirmary, Leicester LE2 7LX, UK;2. Department of Molecular Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK;3. Cancer Research Unit, Children’s Medical Research Institute, University of Sydney, Westmead, NSW, Australia;1. Department of Liberal Arts and Sciences, Kagawa Prefectural University of Health Sciences, Hara 281-1, Mure, Takamatsu, Kagawa 761-0123, Japan;2. Department of Physiology, International University of Health and Welfare School of Medicine, 4-3 Kozu-no-Mori, Narita 286-8686, Japan;3. United Graduate School of Child Development, Osaka University, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan;4. Department of Physical Therapy, Osaka Yukioka College of Health Science, Sojiji 1-1-41, Ibaraki, Osaka 567-0801, Japan;3. From the School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom and;4. School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom;1. Department of Infection Biology, University Hospital Erlangen, Erlangen, Germany;2. Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, Göttingen, Germany;3. Department of Experimental Biomedicine I, University Hospital and Rudolf Virchow Center, University of Würzburg, Würzburg, Germany;1. Mahidol University, Institute of Molecular Biosciences, Nakhon Pathom 73170, Thailand;2. Centre National de la Recherche Scientifique, 2 rue Michel Ange, 75016 Paris, France;1. Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA, USA;2. PhD Program in Virology, Harvard University, Cambridge, MA, USA;3. Department of Medicine, University of Washington, Seattle, WA, USA;4. Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA;5. Department of Global Health, Milken Institute School of Public Health, George Washington University, Washington, DC, USA;6. Nepal Nutrition Intervention Project, Sarlahi, Kathmandu, Nepal;7. Department of Pediatrics, Seattle Children''s Research Institute and University of Washington, Seattle, WA, USA |
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| Abstract: | The present study was undertaken to investigate the interaction of IL-7 and sCD23 on human peripheral blood T cell activation and CTL differentiation. Purified T lymphocytes were stimulated with mitogen plus IL-2 and subcultured for 7 days with IL-7 and/or sCD23. The combination of IL-7 and sCD23 synergistically enhanced the proliferation of both CD4+and CD8+T cells. CD8+T cells, however, were usually more responsive to IL-7 and sCD23. This synergy was observed on both subsets of T cells. Furthermore, these cytokines synergistically augment the CTL activity of CD8+T cells in both mitogen- and antigen-activated T cells. MAbs anti-IL-2 or anti-IL-2R (CD25) and anti-IL-12 had no effect on T cell proliferation and CD8+cytotoxic activity induced by IL-7 and sCD23. We analyzed the effect on IFN-γ induction by CD8+T cells and found that IL-7 alone was incapable of inducing detectable levels of IFN-γ production, but together with sCD23 it enhanced the production of IFN-γ. We also found that IFN-γ was not required for enhanced CTL activity of CD8+T cells, because rabbit anti-IFN-γ did not block the synergistic effects of either cytokine. The data demonstrate that the synergistic stimulatory activity of IL-7 and sCD23 may be of significance in the human CTL development and provide an alternative mechanism of stimulating T cells for use in immunotherapy. |
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