Both tumor necrosis factor-alpha and interferon-gamma are involved in the activation of macrophage cytocidal/cytostatic effector function. Recent studies provide evidence that, in non-septic inflammatory disease, T cells may activate macrophages primed by interferon-gamma either by providing tumor necrosis factor-alpha (in soluble or membrane-anchored form) or by inducing macrophage tumor necrosis factor-alpha production by antigen-non-specific cognate interactions. Conversely, T cells may inhibit macrophage activation by producing cytokines that inhibit either tumor necrosis factor-alpha production or interferon-gamma receptor signaling.