Annual Review of Immunology Volume 23 2005 by Annual Reviews

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Rev. Immunol. 23:23-68. org by HINARI on 08/26/07. For personal use only. Role of OX40 in Alloresponses and Cancer Deficiency in OX40 or OX40L does not alter T cell proliferation in a mixed lymphocyte reaction (MLR) (116, 145) but OX40L–/– DC induce less effector cytokines than WT APC (116) and induce weaker allo-CTL responses (15), consistent with earlier evidence that OX40 is important in alloresponses (163). Similarly, administration of blocking antibodies to OX40L can ameliorate lethal GVHD in mice (164).

Anti-4-1BB therapy of MRL/lpr mice appears to induce deletion of B cells via an IFN-γ -dependent mechanism (218). A similar effect on progressive depletion of B cells is seen in mice constitutively expressing 4-1BBL under the control of an MHC class II promoter (222) or in mice expressing a CD70 transgene (85). These findings suggest that too much costimulation, particularly under conditions of chronic stimulation, can lead to the production of cytokines such as IFN-γ at levels that inhibit cell proliferation.

Thus, its expression pattern suggests that GITR on activated T cells most likely receives signals from GITRL on APCs, early after initial T cell activation. Function of GITR as a Costimulator of Conventional T Cells Evidence for a costimulatory role for GITR on T cells comes from studies of GITRL or anti-GITR stimulation of T cells. Anti-GITR or GITRL can costimulate proliferation of naive, Th1, or Th2 CD4 T cells and CD8 T cells in the presence of suboptimal concentrations of anti-CD3 (41, 42, 295, 297, 299, 300).

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