Regulation of leukocyte recruitment by the long pentraxin PTX3

Deban, Livija; Russo, Remo Castro; Sironi, Marina; Moalli, Federica; Scanziani, Margherita; Zambelli, Vanessa; Cuccovillo, Ivan; Bastone, Antonio; Gobbi, Marco; Valentino, Sonia; Doni, Andrea; Garlanda, Cecilia; Danese, Silvio; Salvatori, Giovanni; Sassano, Marica; Evangelista, Virgilio; Rossi, Barbara; Zenaro, Elena; Constantin, Gabriela; Laudanna, Carlo; ... (2010). Regulation of leukocyte recruitment by the long pentraxin PTX3. Nature immunology, 11(4), pp. 328-34. New York, N.Y.: Nature Publishing Group 10.1038/ni.1854

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Pentraxins are a superfamily of conserved proteins involved in the acute-phase response and innate immunity. Pentraxin 3 (PTX3), a prototypical member of the long pentraxin subfamily, is a key component of the humoral arm of innate immunity that is essential for resistance to certain pathogens. A regulatory role for pentraxins in inflammation has long been recognized, but the underlying mechanisms remain unclear. Here we report that PTX3 bound P-selectin and attenuated neutrophil recruitment at sites of inflammation. PTX3 released from activated leukocytes functioned locally to dampen neutrophil recruitment and regulate inflammation. Antibodies have glycosylation-dependent regulatory effect on inflammation. Therefore, PTX3, which is an essential component of humoral innate immunity, and immunoglobulins share functional outputs, including complement activation, opsonization and, as shown here, glycosylation-dependent regulation of inflammation.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute

UniBE Contributor:

Moalli, Federica

ISSN:

1529-2908

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:11

Last Modified:

04 May 2014 23:05

Publisher DOI:

10.1038/ni.1854

PubMed ID:

20208538

Web of Science ID:

000275849500012

URI:

https://boris.unibe.ch/id/eprint/2163 (FactScience: 204419)

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