NDLI: The killing of Leishmania major by human macrophages is mediated by nitric oxide induced after ligation of the Fc epsilon RII/CD23 surface antigen.

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The killing of Leishmania major by human macrophages is mediated by nitric oxide induced after ligation of the Fc epsilon RII/CD23 surface antigen.

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The killing of Leishmania major by human macrophages is mediated by nitric oxide induced after ligation of the Fc epsilon RII/CD23 surface antigen.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Vouldoukis, I. Mossalayi, M. D. Riveros-moreno, V. Ouaaz, F. Bécherel, P. Moncada, S. Debré, P. Dugas, B.
Description	Author Affiliation: Vouldoukis I ( Centre National de la Recherche Scientifique, Pitié-Salpêtrière Hospital, Paris, France.);
Abstract	Serum IgE concentrations and the expression of the low-affinity receptor for IgE (Fc epsilon RII/CD23) are increased in cutaneous leishmaniasis or after immune challenge with Leishmania antigens. In vitro, the ligation of CD23 by IgE-anti-IgE immune complexes (IgE-IC) or by anti-CD23 monoclonal antibody (mAb) induces nitric oxide (NO) synthase and the generation of various cytokines by human monocytes/macrophages. The present study shows that IgE-IC, via CD23 binding, induce intracellular killing of Leishmania major in human monocyte-derived macrophages through the induction of the L-arginine:NO pathway. This was demonstrated by increased generation of nitrite (NO2-), the stable oxidation product of NO, and by the ability of NG-monomethyl-L-arginine to block both NO generation and parasite killing. A similar NO-dependent effect was observed with interferon gamma-treated cells. Tumor necrosis factor alpha is involved in this process, since both the induction of NO synthase and the killing of parasites caused by anti-CD23 mAb were inhibited by an anti-tumor necrosis factor alpha mAb. Treatment of noninfected CD23+ macrophages with IgE-IC provided protection against subsequent in vitro infection of these cells by Leishmania major promastigotes. Thus, IgE-IC promote killing of L. major by inducing NO synthase in human macrophages.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	92
Language	English
Publisher	National Academy of Sciences
Publisher Date	1995-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amino Acid Oxidoreductases Biosynthesis Cytokines Pharmacology Leishmania Major Immunology Macrophages Nitric Oxide Receptors, IgE Physiology Antagonists & Inhibitors Metabolism Animals Antibodies, Monoclonal Antigens, CD Arginine Analogs & Derivatives Cells, Cultured DNA Primers Gene Expression Interferon-gamma Interleukin-4 Lipopolysaccharides Drug Effects Molecular Sequence Data Nitric Oxide Synthase Phagocytosis Polymerase Chain Reaction RNA, Messenger Recombinant Proteins Superoxides Tumor Necrosis Factor-alpha Omega-N-Methylarginine Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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