COSTIMULATION OF HUMAN CD4(-CELLS BY FIBROBLAST GROWTH-FACTOR-I (ACIDIC FIBROBLAST GROWTH-FACTOR)() T)

T cell infiltration is prevalent in wound healing, atherosclerosis, va scular lesions in chronic allograft rejection, and autoimmune diseases . Whether T cells play a role in the migration and proliferation of va scular smooth muscle cells and endothelial cells in these lesions is n ot known. We previously reported that some human T cells express FGF-1 , a potent growth factor for vascular smooth muscle cells and endothel ial cells. In this study, we extend this observation and examine the e xpression and function of FGF receptors on human T cells. Using revers e transcription-PCR, Northern analysis, and immunohistochemistry, we f ound that some human T cells also express high affinity FGF receptor 1 (FGFR-1) respond to FGF-1, In the presence of anti-CD3, exogenous FGF -1 functions as a costimulator for these T cells, while FGF-1 alone do es not induce T cell proliferation. [H-3]Thymidine incorporation is se venfold higher in T cells costimulated with FGF-1 compared with stimul ation with anti-CD3 alone, Using limiting dilution, we demonstrate tha t FGF-responsive T cells are present in normal peripheral blood at a m ean frequency of 1:19780 (95% confidence limits, 1:15100-1:23000), and similar T cells are increased in the peripheral blood of heart transp lant recipients (mean frequency, 1:4210; 95% confidence limits, 1:3420 -1:6781). In addition, a subline of Jurkat, a human T cell tumor, expr esses FGFR-1 receptor, The function of FGFR-1 receptor in Jurkat T cel ls is demonstrated by the production of IL-2 after stimulation with FG F-1 and anti-CD3, IL-2 levels are sevenfold higher in Jurkat T cells c ostimulated with FGF-1 compared with those stimulated with anti-CD3 al one, FGF-1 alone has no effect on jurkat T cells, These findings thus provide evidence that a subset of human T cells expresses a receptor f or vascular cell growth factors, and this receptor functions to increa se IL-2 production consistent with costimulation. The potential role o f FGF-responsive T cells in a variety of vascular and inflammatory les ions is discussed.