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However, no defect in antibody responses or in the ex vivo CTL activity were observed following VSV-infection of LIGHT–/– mice (252). Thus, there does not appear to be a major requirement for LIGHT in primary antiviral immunity, although this should be further analyzed with other infectious models, particularly at mucosal sites. Role of LIGHT in Allorecognition Several studies have shown that LIGHT pathway blockers, including HVEMIg, anti-HVEM, and DcR3, block MLRs (243, 250, 262). Investigators obtained different results when analyzing alloresponses in the absence of LIGHT, depending on whether the T cells or the APC lack LIGHT.

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.

Infection of mice with influenza virus, CD70 is detected on T cells and B cells in the draining lymph nodes. CD70 is also expressed on T cells in the lung but is largely intracellular, suggesting that CD70 is regulated posttranslationally as well as transcriptionally (18). The expression pattern of CD27 and CD70 suggests that CD27 on T cells may receive signals by binding CD70 on activated B cells, DCs, or through T-T interaction. sgm LaTeX2e(2002/01/18) P1: IKH TNF FAMILY MEMBERS AS COSTIMULATORS 29 Annu.

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