Type 1 interferon (IFNα/β) and type 2 nitric oxide synthase regulate the innate immune response to a protozoan parasite

Andreas Diefenbach, Heike Schindler, Norbert Donhauser, Elke Lorenz, Tamás Laskay, John MacMicking, Martin Röllinghoff, Ion Gresser, Christian Bogdan*

*Corresponding author for this work
288 Citations (Scopus)

Abstract

Type 2 nitric oxide synthase (NOS2) is required for the Th1-dependent healing of infections with intracellular microbes, including Leishmania major. Here, we demonstrate the expression and define the function of NOS2 during the innate response to L. major. At day 1 of infection, genetic deletion or functional inactivation of NOS2 abolished the IFNγ and natural killer cell response, increased the expression of TGFβ, and caused parasite spreading from the skin and lymph node to the spleen, liver, bone marrow, and lung. Induction of NOS2 was dependent on IFNα/β. Neutralization of IFNα/β mimicked the phenotype of NOS2(-/-) mice. Thus, IFNα/β and NOS2 are critical regulators of the innate response to L. major.

Original languageEnglish
JournalImmunity
Volume8
Issue number1
Pages (from-to)77-87
Number of pages11
ISSN1074-7613
DOIs
Publication statusPublished - 01.01.1998

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)

DFG Research Classification Scheme

  • 204-05 Immunology

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