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The Journal of Immunology, Vol 144, Issue 4 1202-1207, Copyright © 1990 by American Association of Immunologists
ARTICLES |
A Pierres, C Cerdan, M Lopez, C Mawas and D Olive
Unite de Cancerologie et Therapeutique Experimentale, U. 119 Inserm, Marseille, France.
We have investigated the role of the CD2 and the CD28 Ag-independent pathways of activation on CD3low thymocytes. We previously showed that anti-CD28 mAb synergized with anti-CD2 mAb directed against epitopes T11.1 and T11.2, in the activation of purified resting T cells or unseparated thymocytes. Proliferation induced via CD2 plus CD28 was mediated via an IL-2-dependent pathway and was not affected by prior modulation of the CD3-TCR complex. Here, we show that a subset of CD3low thymocytes, although unresponsive to CD3 activation, can be activated to proliferate through the CD2 or the CD28 pathways, in the presence of exogenous IL-2. The mitogenic combination of mAb to CD2 and CD28 induces a proliferation of thymocytes which, in absence of exogenous lymphokines, is restricted to the more mature intrathymic subpopulation, CD1a-. However, CD3low thymocytes can also be triggered through the CD2 plus CD28 activation pathways but require at least addition of exogenous IL-2 to proliferate. This study demonstrates that a fraction of immature CD3low thymocytes possesses functional CD2 and CD28 surface molecules at a time when CD3 is not yet functional.
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C. S. Heinly, G. D. Sempowski, D. M. Lee, D. D. Patel, P. M. McDermott, R. M. Scearce, C. B. Thompson, and B. F. Haynes Comparison of thymocyte development and cytokine production in CD7-deficient, CD28-deficient and CD7/CD28 double-deficient mice Int. Immunol., February 1, 2001; 13(2): 157 - 166. [Abstract] [Full Text] [PDF] |
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