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  • Systemic but not local infections elicit immunosuppressive IL-10 production by natural killer cells.

Systemic but not local infections elicit immunosuppressive IL-10 production by natural killer cells.

Cell host & microbe (2009-12-17)
Georgia Perona-Wright, Katja Mohrs, Frank M Szaba, Lawrence W Kummer, Rajat Madan, Christopher L Karp, Lawrence L Johnson, Stephen T Smiley, Markus Mohrs
ABSTRACT

Surviving infection represents a balance between the proinflammatory responses needed to eliminate the pathogen, and anti-inflammatory signals limiting damage to the host. IL-10 is a potent immunosuppressive cytokine whose impact is determined by the timing and localization of release. We show that NK cells rapidly express IL-10 during acute infection with diverse rapidly disseminating pathogens. The proinflammatory cytokine IL-12 was necessary and sufficient for NK cell induction of IL-10. NK cells from mice with systemic parasitic infection inhibited dendritic cell release of IL-12 in an IL-10-dependent manner, and NK cell depletion resulted in elevated serum IL-12. These data suggest an innate, negative feedback loop in which IL-12 limits its own production by eliciting IL-10 from NK cells. In contrast to disseminating pathogens, locally restricted infections did not elicit NK cell IL-10. Thus systemic infections uniquely engage NK cells in an IL-10-mediated immunoregulatory circuit that functions to alleviate inflammation.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Lipopolysaccharides from Escherichia coli O111:B4, purified by phenol extraction
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Lipopolysaccharides from Escherichia coli O111:B4, γ-irradiated, BioXtra, suitable for cell culture
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Lipopolysaccharides from Escherichia coli O111:B4, Ready Made solution, 1 mg/mL
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Lipopolysaccharides from Escherichia coli O111:B4, purified by gel-filtration chromatography
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Lipopolysaccharides from Escherichia coli O111:B4, purified by trichloroacetic acid extraction
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Lipopolysaccharides from Escherichia coli O111:B4, FITC conjugate
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