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Clin Immunol. 2014 Feb;150(2):153-60. doi: 10.1016/j.clim.2013.11.010. Epub 2013 Nov 27.

IL-10 suppresses IL-17-mediated dermal inflammation and reduces the systemic burden of Vaccinia virus in a mouse model of eczema vaccinatum.

Author information

1
Department of Pediatrics, Boston Children's Hospital, Boston, MA 02115, USA.
2
Department of Pediatrics, Boston Children's Hospital, Boston, MA 02115, USA. Electronic address: hans.oettgen@childrens.harvard.edu.

Abstract

Individuals with atopic dermatitis (AD) are susceptible to a severe, potentially fatal, systemic infection and inflammatory response following exposure to Vaccinia virus (VV). IL-10 acts both as an inducer of Th2 responses and as a regulator of T cell activation. It has been shown to limit skin inflammation elicited by contact sensitizers. AD exacerbations have been associated with decreased IL-10 function. We used IL-10(-/-) mice to test the role of the cytokine in VV immunity. They exhibited larger primary lesions and increased cutaneous neutrophil infiltration compared to wild-type (WT) counterparts. This was associated with enhanced production of IL-17A, IL-17F and CXCL2. Paradoxically, despite intact adaptive immune responses, tissue viral burdens were increased in IL-10(-/-) mice. These findings suggest that IL-10 is important in limiting skin inflammation induced by VV and that abnormal IL-17-driven neutrophil recruitment at the primary infection site in the skin results in increased systemic viral dissemination.

KEYWORDS:

Atopic dermatitis; Eczema vaccinatum; Vaccine

PMID:
24412909
PMCID:
PMC3946343
DOI:
10.1016/j.clim.2013.11.010
[Indexed for MEDLINE]
Free PMC Article

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