Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0905493

Received for publication September 2, 2005.
Revised October 21, 2005.
Accepted for publication November 21, 2005.

Article

Regulation of PTX3, a key component of humoral innate immunity in human dendritic cells: stimulation by IL-10 and inhibition by IFN-{gamma}

Andrea Doni *, Mosca Michela {dagger}, Barbara Bottazzi *, Giuseppe Peri *, Sonia Valentino *, Nadia Polentarutti *, Cecilia Garlanda *, and Alberto Mantovani *{ddagger}@

*Istituto Clinico Humanitas (ICH), Rozzano, Milan, Italy; {dagger}Department of Experimental Medicine and Public Health, University of Camerino, Macerata, Italy; and {ddagger}Institute of General Pathology, University of Milan, Italy

@ To whom correspondence should be addressed. E-mail: mantovani{at}humanitas.it.


  Abstract

The protopypic long pentraxin 3 (PTX3) is a unique, humoral pattern-recognition receptor, which plays a nonredundant function in innate resistance to pathogens. Dendritic cells (DC) of myelomonocytic origin, but not plasmacytoid DC, are a major source of PTX3 in response to Toll-like receptor (TLR) engagment. The present study was designed to explore the regulation of PTX3 production in DC. PTX3 production was induced by TLR ligands, CD40 ligand, and interleukin (IL)-1{beta} and was suppressed by dexamethasone, 1{alpha}, 25-dihydroxivitamin D3, and prostaglandin E2. It was unexpected that lipopolysaccharide (LPS)-stimulated PTX3 production was enhanced by IL-10 and inhibited by IL-4 and interferon-{gamma} (IFN-{gamma}). Enhancement of PTX3 production by IL-10 was also evident when Pam3 Cys-Ser-(Lys)4 .3HCl, a TLR2-TLR1 agonist, polyionisicpolycytidylic acid, a TLR3 agonist, and IL-1{beta} were used as stimuli. The effect of IL-10 was blocked by an anti-IL-10 monoclonal antibody (mAb) or an anti-IL-10 receptor {alpha} mAb, which also reduced the LPS-induced production. Thus, production of PTX3 in DC is subjected to a distinct regulatory network, with inhibition by IFN-{gamma} and enhancement by IL-10. The amplification by IL-10 of production of a nonredundant component of fluid-phase innate immunity mirrors the IL-10 stimulatory function on B cells in adaptive immunity. As PTX3 is also an extracellular matrix component, IL-10-enhanced PTX3 production may play a role in orchestration of tissue remodeling in chronic inflammation.

Key Words: pentraxins • cytokines • tissue remodeling




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