Macrophage activation by T cells: cognate and non-cognate signals.
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.
James H. Quillen College of Medicine, East Tennessee State University, Johnson City.
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D000818:Animals; D002450:Cell Communication; D006801:Humans; D007249:Inflammation; D007371:Interferon-gamma / Q000502:physiology; D007378:Interleukins / Q000502:physiology; D008262:Macrophage Activation; D008565:Membrane Proteins / Q000502:physiology; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor; D015398:Signal Transduction / Q000502:physiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D007378:Interleukins; D008565:Membrane Proteins; D011956:Receptors, Cell Surface; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D007371:Interferon-gamma