The Journal of experimental medicine, 1996
Department of Neurobiology and Anatomy
Drexel University College of Medicine
2900 W. Queen Lane, Room186
Tai, X., Yashiro, Y., Abe, R., Toyooka, K., Wood, C., Morris, J., … Fujiwara, H. (1996). A role for CD9 molecules in T cell activation. The Journal of Experimental Medicine.
Tai, X., Y. Yashiro, R. Abe, K. Toyooka, C. Wood, J. Morris, A. Long, et al. “A Role for CD9 Molecules in T Cell Activation.” The Journal of experimental medicine (1996).
Tai, X., et al. “A Role for CD9 Molecules in T Cell Activation.” The Journal of Experimental Medicine, 1996.
Costimulation mediated by the CD28 molecule plays an important role in optimal activation of T cells. However, CD28-deficient mice can mount effective T cell-dependent immune responses, suggesting the existence of other costimulatory systems. In a search for other costimulatory molecules on T cells, we have developed a monoclonal antibody (mAb) that can costimulate T cells in the absence of antigen-presenting cells (APC). The molecule recognized by this mAb, 9D3, was found to be expressed on almost all mature T cells and to be a protein of approximately 24 kD molecular mass. By expression cloning, this molecule was identified as CD9, 9D3 (anti-CD9) synergized with suboptimal doses of anti-CD3 mAb in inducing proliferation by virgin T cells. Costimulation was induced by independent ligation of CD3 and CD9, suggesting that colocalization of these two molecules is not required for T cell activation. The costimulation by anti-CD9 was as potent as that by anti-CD28. Moreover, anti-CD9 costimulated in a CD28- independent way because anti-CD9 equally costimulated T cells from the CD28-deficient as well as wild-type mice. Thus, these results indicate that CD9 serves as a molecule on T cells that can deliver a potent CD28- independent costimulatory signal.