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

doi:10.1016/S1074-7613(00)80460-4

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^*

^*Korrespondierende/r Autor/-in für diese Arbeit

Klinik für Infektiologie und Mikrobiologie

288 Zitate (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.

Originalsprache	Englisch
Zeitschrift	Immunity
Jahrgang	8
Ausgabenummer	1
Seiten (von - bis)	77-87
Seitenumfang	11
ISSN	1074-7613
DOIs	https://doi.org/10.1016/S1074-7613(00)80460-4
Publikationsstatus	Veröffentlicht - 01.01.1998

Strategische Forschungsbereiche und Zentren

Forschungsschwerpunkt: Infektion und Entzündung - Zentrum für Infektions- und Entzündungsforschung Lübeck (ZIEL)

DFG-Fachsystematik

2.21-05 Immunologie

UN SDGs

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10.1016/S1074-7613(00)80460-4

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

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.",

author = "Andreas Diefenbach and Heike Schindler and Norbert Donhauser and Elke Lorenz and Tam{\'a}s Laskay and John MacMicking and Martin R{\"o}llinghoff and Ion Gresser and Christian Bogdan",

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T1 - Type 1 interferon (IFNα/β) and type 2 nitric oxide synthase regulate the innate immune response to a protozoan parasite

AU - Diefenbach, Andreas

AU - Schindler, Heike

AU - Donhauser, Norbert

AU - Lorenz, Elke

AU - Laskay, Tamás

AU - MacMicking, John

AU - Röllinghoff, Martin

AU - Gresser, Ion

AU - Bogdan, Christian

PY - 1998/1/1

Y1 - 1998/1/1

N2 - 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.

AB - 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.

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U2 - 10.1016/S1074-7613(00)80460-4

DO - 10.1016/S1074-7613(00)80460-4

M3 - Journal articles

C2 - 9462513

AN - SCOPUS:0031907920

SN - 1074-7613

VL - 8

SP - 77

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JO - Immunity

JF - Immunity

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

Abstract

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