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Conversely, transgenic expression of OX40L in C57BL/6 mice, which normally control Leishmania, resulted in an elevated Th2 response and decreased parasite clearance (138). Role of OX40/OX40L in Autoimmune and Inflammatory Reactions A large body of evidence suggests that OX40-OX40L interactions play a role in autoimmunity and inflammation. OX40-OX40L interaction is required for the induction of EAE in mice, and depletion of OX40+ T cells or preventing OX40OX40L interactions ameliorates disease (121, 129, 154, 155).

The absence of OX40 does not in itself appear to induce tolerance (159). However, provision of agonistic anti-OX40 can reverse T cell anergy induced in vivo by peptide administration (161). Interestingly, transfer of self-specific CD4 T cells into recipient mice induces expansion of T cells, which remain anergic. However, concomitant administration of agonistic anti-OX40 antibodies relieves these self-specific T cells from their anergic state, resulting in autoimmunity and death of the anti-OX40-treated recipient mice (162).

On T cells, constitutive overexpression of OX40L results in accumulation of CD4 effector T cells, increased CD4 T cell responses, as well as an autoimmune phenotype characterized by inflammation of the lung and intestine, with no change in CD8 populations (148). Thus, both gene-targeted and transgenic mice support a role for OX40 primarily on CD4 T cells. There are conflicting data on the effect of OX40 or OX40L deficiency on B cell responses in mice. Three studies showed no defect in antibody responses to both protein and infectious agents (KLH, VSV, influenza virus, L.

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