The inflammatory cytokine IL-6 contributes to immune activation that causes acute and chronic rejection of organ transplants. However, very little is known about the signaling mechanisms by which IL-6 functions in this setting. IL-6 can transduce signals that lead to distinct biological outcomes through mechanisms that are either dependent or independent of IL-6 receptor (IL-6R) expression on the surface of target cells. Using mice that lack IL-6R expression only in T cells (IL-6R-TKO) and a murine aortic interposition model of vascular rejection, we examined the role of IL-6R in T cells on allogeneic immune responses. IL-6R-TKO mice were generated by crossing IL-6Rflox/flox mice with CD4-Cre partners. IL-6R expression was absent in T cells from IL-6R-TKO mice but remained abundant on other leukocyte lineages. There was no difference in the accumulation of CD4 and CD8 T cells in allograft arteries from IL-6R-TKO graft recipients as compared to IL-6Rflox/flox control counterparts. IL-6R expression on T cells also did not affect the accumulation of macrophages in allograft arteries. When donor-specific antibodies (DSA) were examined, their de novo generation was apparent 2 – 3 weeks after transplantation, remained high thereafter, and was markedly and significantly reduced in IL-6R-TKO graft recipients as compared to controls. Overall, our findings indicate that IL-6R expression in T cells is dispensable for the development of peripheral effector T cell responses towards vascular allografts but is needed for the development of DSA.