The increased risk of mortality associated with sepsis and sepsis shock may be attributed to the immunosuppressive functions of Tregs by: (a) directly inhibiting effector CD4+ T cell proliferation and cytokine secretion (124–126); (b) indirectly supressing APC/T-cell receptor mediated CD4+ and CD8+ T cell activation (125–127); (c) suppressing T cell activation through increased expression of programmed cell death-1 (PD-1) receptor (128); or (d) suppressing other immune effector cells such as natural killer cells, B cells, and monocytes (129–131). Here, CD4 is linked to Sepsis.