Effect of IL‐4 and IL‐13 on IFN‐γ‐induced production of nitric oxide in mouse macrophages infected with herpes simplex virus type 2

FEBS Letters

Lovmand, Jette¹  Mogensen, Søren C.¹  Ellermann-Eriksen, Svend¹  Paludan, Søren R.¹ 

[1]Department of Medical Microbiology and Immunology, The Bartholin Building, University of Aarhus, DK-8000 Aarhus C, Denmark

关键词: Interleukin-4;    Interleukin-13;    Interferon-γ;    Herpes simplex virus;    Macrophage;    Nitric oxide;    IFN-γ;    interferon-γ;    IL-4;    interleukin-4;    IL-13;    interleukin 13;    TNF-α;    tumor necrosis factor-α;    NO;    nitric oxide;    iNOS;    inducible nitric oxide synthase;    HSV-2;    herpes simplex virus type 2;    IRF;    interferon regulatory factor;    STAT;    signal transducer and activator of transcription;    NF-κB;    nuclear factor-κB;    Jak;    Janus kinase;    Th;    T-helper cell;    RT-PCR;    reverse transcribed-polymerase chain reaction;   

DOI  :  10.1016/S0014-5793(97)00987-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Interleukin (IL)-4 and IL-13 share a wide range of activities. Prominent among these is the ability to antagonize many interferon (IFN)-γ-induced activities. Here we demonstrate that IL-4 and IL-13 totally abrogate IFN-γ-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) mRNA and protein synthesis in a murine macrophage cell line. IFN-γ-treated cells infected with herpes simplex virus type 2 (HSV-2) or costimulated with tumor necrosis factor (TNF)-α showed an enhanced reactivity, which was only partially reduced by IL-4/13. The results indicate that IL-4 and IL-13 function by intervening with a step prior to iNOS transcription by antagonizing IFN-γ-induced signal(s) without counteracting synergistic virus- or TNF-α-induced signals. The beneficial effect of a sustained NO production in foci of virus infection is suggested.

【 授权许可】

Unknown