Macrophage priming by interferon gamma: a selective process with potentially harmful effects.
Macrophage priming by interferon gamma: a selective process with potentially harmful effects.
复制标题
干扰素γ启动巨噬细胞：具有潜在有害影响的选择性过程。
DOI：
10.1002/jlb.52.6.579
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发表时间：
1992
影响因子：
5.5
通讯作者：
Maier,RV
中科院分区：
文献类型：
--
作者：
Williams,JG;Jurkovich,GJ;Hahnel,GB;Maier,RV
The tissue-fixed macrophage is a key cellular element in the initiation and regulation of inflammation. Understanding the regulation of macrophage activation may provide valuable clues to the mechanisms involved in both beneficial and deleterious effects of inflammation. The lymphokine interferon-γ (IFN-γ) is capable of producing paradoxical immunoinflammatory effects. In the immunocompromised host it up-regulates a variety of immune functions and improves survival, but it is also capable of producing harmful effects by sensitizing immunocompetent animals to subclinical doses of endotoxin. These paradoxical effects suggest that the state of activation or priming of the host immune system is a key determinant of its response to endotoxemia. Because tumor necrosis factor (TNF) and procoagulant activity (PCA) elaboration by the tissue-fixed macrophage play a central role in the host response to endotoxin, we asked whether the paradoxical effects of IFN-γ may be caused by priming of the macrophage for TNF and/or PCA production. In vitro, IFN-γ produces a marked augmentation in TNF but does not alter PCA elaboration in response to endotoxin, demonstrating the selectivity of IFN-γ priming of the macrophage. In vivo, IFN-γ pre- treatment followed by an established subclinical endotoxin exposure enhances toxicity while simultaneously increasing peak serum TNF levels. Exogenous priming by IFN-γ alters the activation state of the macrophage and modifies the host response to endotoxin. Because this response is also dependent on the host's underlying immune state, IFN-γ treatment in the immunocompetent host has the potential to produce deleterious effects by eliciting an exaggerated TNF response during endotoxemia.
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T细胞分化抗原和Ia在大鼠细胞毒性T淋巴细胞上的表达。
影响因子：
4.4
作者：
A. Duarte;C. Carpenter;T. Strom
通讯作者：
T. Strom
DOI：
--
发表时间：
1977
期刊：
影响因子：
--
作者：
Guttmann Rd
通讯作者：
Guttmann Rd
细胞毒性 T 细胞在介导首次同种异体移植排斥反应中的可能作用。
影响因子：
6.2
作者：
B. Hall;K. Gurley;S. Dorsch
通讯作者：
S. Dorsch
带血管器官同种异体移植物的排斥和延长机制
影响因子：
8.7
作者：
N. Tilney;Jerzy W. Kupiec;C. D. Heidecke;Lear Pa;T. B. Strom
通讯作者：
T. B. Strom
介导小鼠移植排斥的细胞。
影响因子：
15.3
作者：
B E Loveland;P. M. Hogarth;R. Ceredig;I. F. McKenzie
通讯作者：
I. F. McKenzie