[PDF][PDF] Type 1 interferon (IFNα/β) and type 2 nitric oxide synthase regulate the innate immune response to a protozoan parasite
A Diefenbach, H Schindler, N Donhauser, E Lorenz… - Immunity, 1998 - cell.com
A Diefenbach, H Schindler, N Donhauser, E Lorenz, T Laskay, J MacMicking, M Röllinghoff…
Immunity, 1998•cell.comType 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 …
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 …
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.
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