Current understanding of macrophage type 1 cytokine responses during intracellular infections
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Z. Xing [1]
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[1] McMaster University
McMaster University
Canadá
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- Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 15, Nº. 1, 2000, págs. 199-205
- Idioma: inglés
- Enlaces
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Resumen
Macrophages are important effector cells in cell-mediated immunity against intracelllular infection.
Among cytokines that macrophages are able to release are IL-12 and TNFa. IL-12 is a critical linker between the innate and adaptive cell-mediated immunity, capable of T h I differentiation and IFNy release by T and NK cells. IFNy is critically required for the activation of macrophage bactericidal activities. Recently emerging evidence suggests that macrophages are able to release not only IL-12 and TNFa but also IFNy. However, the mechanisms that control the release of each of these type I cytokines in macrophages appear different. While macro phages release TNFa in an indiscriminate and IL12-independent way , the release of IL-12, particularly bioactive IL-12 p70, and IFNy is under tight control. We are just beginning to understand what controls the release of IL-12 p70, a question of fundamental importance to understanding the mechanisms underlying the initiation of cell-mediated immunity. Our recent findings have shed more insights into the regulatory mechanisms of macrophage IFNy responses. It has become evident that IL-12 is required not only for T h I differentiation but also for IFNy responses by both T cells and macrophages during intracellular infection. In this overview, we have discussed about the current understanding of the regulation of macrophage type I cytokine responses during intracellular infection , based upon the recent findings from us and others.
