It has been shown previously that C3a and C5a both activate T cells and antigen-presenting cells (APC), and that signaling of C3aR/C5aR on T cells and APCs influences T cell differentiation, expansion and survival of CD4+ T helper cells, which suggests that complement deficiency or blockade can potentially attenuate T cell-mediated autoimmunity (T regulatory and T effector cell balance) and thus delay allograft rejection (38). The gene discussed is C5AR1; the disease is Autoimmunity.