Stout R D
James H. Quillen College of Medicine, East Tennessee State University, Johnson City.
Curr Opin Immunol. 1993 Jun;5(3):398-403. doi: 10.1016/0952-7915(93)90059-2.
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.
肿瘤坏死因子-α和干扰素-γ均参与巨噬细胞杀细胞/细胞抑制效应功能的激活。最近的研究表明,在非脓毒症性炎症疾病中,T细胞可能通过提供肿瘤坏死因子-α(以可溶性或膜锚定形式)或通过抗原非特异性同源相互作用诱导巨噬细胞产生肿瘤坏死因子-α,从而激活由干扰素-γ启动的巨噬细胞。相反,T细胞可能通过产生抑制肿瘤坏死因子-α产生或干扰素-γ受体信号传导的细胞因子来抑制巨噬细胞的激活。