Interleukin-10 (IL-10) is a multifunctional cytokine with diverse effects on most hematopoietic cell types. It appears the principal function of IL-10 is to limit and ultimately terminate inflammatory response. We demonstrate here that interferon-alpha2b (IFN-alpha) increases the expression of IL-10 in activated primary CD8(+) T cells. Optimal induction of mRNA expression and protein synthesis was observed when IFN-alpha was added to cells activated by the combination of anti-CD3 monoclonal antibody (mAb) and IL-2. Maximal stimulation of IL-10 protein production was observed after prolonged incubation periods (48-72 h). No effects were observed on the production of IL-4, whereas IFN-gamma was produced with a faster kinetics than an untreated control. Our data indicate that IFN-alpha promotes the development of a CD8(+) T cell population with enhanced anti-inflammatory activity, which may play a critical role in the regulation of a proper immune response.

IFN-alpha2b increases interleukin-10 expression in primary activated human CD8+ T cells

SECCHIERO, Paola;
2002

Abstract

Interleukin-10 (IL-10) is a multifunctional cytokine with diverse effects on most hematopoietic cell types. It appears the principal function of IL-10 is to limit and ultimately terminate inflammatory response. We demonstrate here that interferon-alpha2b (IFN-alpha) increases the expression of IL-10 in activated primary CD8(+) T cells. Optimal induction of mRNA expression and protein synthesis was observed when IFN-alpha was added to cells activated by the combination of anti-CD3 monoclonal antibody (mAb) and IL-2. Maximal stimulation of IL-10 protein production was observed after prolonged incubation periods (48-72 h). No effects were observed on the production of IL-4, whereas IFN-gamma was produced with a faster kinetics than an untreated control. Our data indicate that IFN-alpha promotes the development of a CD8(+) T cell population with enhanced anti-inflammatory activity, which may play a critical role in the regulation of a proper immune response.
2002
Curreli, S; Romerio, F; Secchiero, Paola; Zella, D.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1208720
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