Annual Review of Immunology Volume 23 2005 by Annual Reviews

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Immunol. 23:23-68. org by HINARI on 08/26/07. For personal use only. TNF FAMILY MEMBERS AS COSTIMULATORS 27 protein kinase (JNK/SAPK) and p38 MAPK cascades (reviewed in 21, 22). CD27, 4-1BB, and GITR have also been shown to activate p38 and JNK in primary cells (36, 43–45). TRAF1, which lacks the RING finger domain required for NF-κB activation, functions to sustain TRAF2 signaling in the CD40 signaling pathway (46) and is also required for maximal 4-1BB-dependent signaling in T cells (C. Srokowski, G.

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. In support of this idea, Myers et al. (223) found that anti-4-1BB stimulation of adoptively transferred CD8 T cells in the presence of Toll-receptor triggering (LPS) resulted in profound expansion of CD8 T cells, which in turn led to suppression of CD4 T cell proliferation by a TGF-β-dependent mechanism.

Blocking of HVEM-LIGHT interaction using HSV-1 glycoprotein D, antiHVEM, or HVEM-Ig inhibits the proliferation of purified T cells responding to anti-CD3 or anti-CD3/CD28 (248–250). Furthermore, two studies showed that purified LIGHT–/– T cells have decreased responses to anti-CD3 alone, consistent with HVEM-LIGHT interactions during T-T interaction enhancing proliferation (251, 252). Although a third study did not show any defect in proliferation of LIGHT−/− T cells (253), this may reflect lower cell densities in the cultures leading to less efficient T-T contact.

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