Journal ArticleDOI
Interleukin-10 (IL-10) inhibits the induction of nitric oxide synthase by interferon-γ in murine macrophages
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TLDR
It is demonstrated that IL-10, a product of Th2 (helper T lymphocyte 2) cells, can antagonise the function of IFN-gamma, a products of Th1 cells, by modulating the mechanism of synthesis of nitric oxide in the macrophages.About:
This article is published in Biochemical and Biophysical Research Communications.The article was published on 1992-02-14. It has received 386 citations till now. The article focuses on the topics: Nitric oxide & Nitric oxide synthase.read more
Citations
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Journal ArticleDOI
Interleukin-10 and the interleukin-10 receptor.
TL;DR: Findings that have advanced the understanding of IL-10 and its receptor are highlighted, as well as its in vivo function in health and disease.
Journal ArticleDOI
Macrophage cytokines: involvement in immunity and infectious diseases.
TL;DR: The functions of cytokines secreted by macrophages are discussed, and what is known about their release mechanisms are summarized to delve into how selected pathogens subvert cytokine release for their own survival.
Journal Article
Inflammatory mediators of asthma: an update.
Journal ArticleDOI
Cytokines in asthma
Kian Fan Chung,Peter J. Barnes +1 more
TL;DR: It is apparent that there is a wide pleiotropy and element of redundancy in the cytokine family in that each cytokine has many overlapping functions, with each function potentially mediated by more than one cytokine.
Journal ArticleDOI
Reciprocal regulation of the nitric oxide synthase/arginase balance in mouse bone marrow‐derived macrophages by TH 1 and TH 2 cytokines
TL;DR: The induction of arginase is tested in bone marrow‐derived macrophages by endogenous mediators that are known to induce NO synthase, or suppress the induction of this enzyme, such as interleukin (IL)‐4, IL‐10, and prostaglandin E2 (PGE2).
References
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Journal ArticleDOI
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor
TL;DR: NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator.
Journal ArticleDOI
Two types of mouse T helper cell. IV. Th2 clones secrete a factor that inhibits cytokine production by Th1 clones.
TL;DR: Biochemical characterization, mAbs, and recombinant or purified cytokines showed that CSIF is distinct from IL-1,IL-2, IL-3, IFN-gamma, GM-CSF, TGF-beta, TNF, LT, and P40, and the potential role of CSIF in crossregulation of Th1 and Th2 responses is discussed.
Journal Article
Release of reactive nitrogen intermediates and reactive oxygen intermediates from mouse peritoneal macrophages. Comparison of activating cytokines and evidence for independent production.
TL;DR: Testing as a sole agent, IFN-gamma was the only one of the 12 cytokines capable of inducing both NO2- and H2O2 release and the pathways leading to secretion of H2 O2 and No2- are independent.
Journal ArticleDOI
Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression.
R de Waal Malefyt,John B. A. G. Haanen,H Spits,M G Roncarolo,A.A. te Velde,Carl G. Figdor,K E Johnson,Rob A. Kastelein,Hans Yssel,J E de Vries +9 more
TL;DR: It is indicated that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.
Journal Article
IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Th1 cells.
David Fiorentino,Albert Zlotnik,Pedro L. Vieira,Tim R. Mosmann,M Howard,Kevin W. Moore,Anne O'Garra +6 more
TL;DR: IL-10 may inhibit macrophage accessory cell function which is independent of TCR-class II MHC interactions, as well as inhibits IL-2-induced IFN-gamma production by Th1 cells in an Ag-free system requiring only the presence of accessory cells.