Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Gobl, Anders; Alm, Gunnar V.

doi:10.1111/j.1365-3083.1992.tb02847.x

Cited by 17 publications

(4 citation statements)

References 39 publications

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“…This indicates that the IFN-a response in different types of leucocytes may be differentially affected by type 2 cytokines. Our results agree with those of other authors who described a down-regulation of IFN-a/b production by IL-4 in PBMC, monocytes and macrophages and by IL-13 in monocytes [41][42][43][44]. However, it has been reported that IL-4 affected IFN-a response in PBMCs stimulated by SV but not by HSV-1 [23].…”

Section: Cytokines and Ifn-a In Hiv-1 Infection 439supporting

confidence: 92%

Production of Interleukin‐4, Interferon (IFN)‐γ and IFN‐α in Human Immunodeficiency Virus‐1 Infection: An Imbalance of Type 1 and Type 2 Cytokines may Reduce the Synthesis of IFN‐α

Hober¹,

Benyoucef²,

Chehadeh³

et al. 1998

Scand J Immunol

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Interferon‐α (IFN‐α) is an important molecule in the antiviral response, but cells from HIV‐1‐infected individuals show a reduced ability to secrete IFN‐α. We investigated an association between an imbalance of type 1/type 2 cytokines and the production of IFN‐α in HIV‐1 infection. We used whole blood culture to study the cytokine production profile, interferon‐γ (IFN‐γ) and interleukin‐4 (IL‐4), in response to HIV‐1 antigens and to study the Sendai Virus and HSV‐1‐induced‐production of IFN‐α in seven HIV‐1‐infected patients. An impaired synthesis of IFN‐α was obtained in patients with a predominant IL‐4 production (IL‐4 > IFN‐γ), and we found a positive correlation between the ex vivo production of IFN‐α and the IFN‐γ/IL‐4 ratio but not with the HIV RNA copy number in plasma. We investigated the role of T‐cell‐derived cytokines in the in vitro production of IFN‐α by PBMC from eight healthy donors, activated with Sendai Virus or HSV‐1. Whereas type 2 cytokines (IL‐4, IL‐13) inhibited virus‐induced IFN‐α synthesis, on the contrary, type 1 cytokines (IL‐2, IFN‐γ) enhanced it. A disarray in the T‐cell‐derived cytokine response may play a role in the defect of IFN‐α production in HIV‐1‐infected individuals. Further investigations are needed to explore this hypothesis.

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Section: Cytokines and Ifn-a In Hiv-1 Infection 439supporting

confidence: 92%

Production of Interleukin‐4, Interferon (IFN)‐γ and IFN‐α in Human Immunodeficiency Virus‐1 Infection: An Imbalance of Type 1 and Type 2 Cytokines may Reduce the Synthesis of IFN‐α

Hober¹,

Benyoucef²,

Chehadeh³

et al. 1998

Scand J Immunol

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“…Also, the production of IL-12 by murine DC is inhibited by IL-4 and IL-10 [7]. These cytokines impair the IFN-a/b responses induced by HSV and SV in human leucocytes [41,42]. In the present study we found, however, no effect of IL-4 and IL-10 on the HSV-induced IFN-a/b responses in the DC lines.…”

Section: Discussioncontrasting

confidence: 52%

Production of Interferon‐α/β by Murine Dendritic Cell Lines Stimulated by Virus and Bacteria

Eloranta¹,

Sandberg²,

Ricciardi‐Castagnoli

et al. 1997

Scand J Immunol

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The interferon-alpha and -beta (IFN-alpha/beta) producing ability of the two murine dendritic cell (DC) lines D2SC/1 and FSDC was studied. The D2SC/1 cells produced IFN-alpha and -beta when stimulated by herpes simplex virus (HSV), Sendai virus (SV) or by the bacteria Escherichia coli or Staphylococcus aureus Cowan I. Precultivating (priming) D2SC/1 cells with recombinant IFN-beta or a combination of IFN-beta and granulocyte-macrophage colony-stimulating factor increased production of IFN-alpha/beta induced by HSV or the bacteria, but not by SV. Also, the kinetics of IFN-alpha/beta responses were different for SV compared to HSV and the bacteria, suggesting different induction mechanisms. The FSDC cells differed from the D2SC/1 cells mainly in that predominantly IFN-beta was produced, that little or no IFN-alpha/beta production was induced by the bacteria, and that the IFN-alpha/beta responses were most efficiently primed by IFN-gamma. Priming the DC lines with tumour necrosis factor-alpha, interleukin-10 (IL-10) or IL-4 did not affect the IFN-alpha/beta response induced by HSV. The results show that the two DC lines provide a convenient tool to study the induction and control of the IFN-alpha/beta response, as well as the immunoregulatory role of IFN-alpha/beta produced by DC.

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“…Another key regulator of cytokine expression in myeloid cells is IL-4 (30). It inhibits virus-induced IFN-␣ production (42)(43)(44) and modulates expression of IL-12 (45,46). IL-4 is also involved in the regulation of IL-12-and IL-18-induced IFN-␥ production (47), but its role in suppressing IL-12 or IL-18 expression during virus infections is still inadequately characterized.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Virus-Induced IL-12 and IL-23 Expression in Human Macrophages

Pirhonen

Matikainen

Julkunen

2002

The Journal of Immunology

121

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IL-23 is a novel cytokine that promotes the proliferation of naive and memory T cells and stimulates their IFN-gamma production. Besides functional similarities, IL-23 bears structural resemblance to IL-12. Biologically active IL-23 is a heterodimer whose p40 subunit is identical to IL-12p40 while its p19 subunit is distantly related to IL-12p35. In the present study we demonstrate that human monocyte-derived macrophages are able to produce IL-23 in response to virus infection. Sendai virus stimulates the expression of p19 and p40 mRNAs in macrophages. Furthermore, it enhances p35 mRNA expression and the production of IL-12. Influenza A virus, in contrast, fails to stimulate IL-12 or IL-23 expression in macrophages. IL-12 and IL-23 contribute to the IFN-gamma-inducing activity that cell culture supernatant from Sendai virus-infected macrophages show in NK-92 cells. The induction of IFN-gamma production occurs in concert with IFN-alphabeta and IL-18, which are also secreted from the virus-infected cells. The IFN-gamma-inducing activity is inhibited by IL-4, which down-regulates the transcription of p19 and p40 genes and the secretion of IFN-alphabeta, IL-12, and IL-18. IFN-gamma, in contrast, up-regulates the p19 and p40 mRNA expression in Sendai virus infection. Thus, IL-4 and IFN-gamma serve as opposing factors in the regulation of IFN-gamma-inducing cytokines, including IL-23, in macrophages.

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Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Cited by 17 publications

References 39 publications

Production of Interleukin‐4, Interferon (IFN)‐γ and IFN‐α in Human Immunodeficiency Virus‐1 Infection: An Imbalance of Type 1 and Type 2 Cytokines may Reduce the Synthesis of IFN‐α

Production of Interleukin‐4, Interferon (IFN)‐γ and IFN‐α in Human Immunodeficiency Virus‐1 Infection: An Imbalance of Type 1 and Type 2 Cytokines may Reduce the Synthesis of IFN‐α

Production of Interferon‐α/β by Murine Dendritic Cell Lines Stimulated by Virus and Bacteria

Regulation of Virus-Induced IL-12 and IL-23 Expression in Human Macrophages

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