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      The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps

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          Abstract

          The long pentraxin (PTX) 3 is produced by macrophages and myeloid dendritic cells in response to Toll-like receptor agonists and represents a nonredundant component of humoral innate immunity against selected pathogens. We report that, unexpectedly, PTX3 is stored in specific granules and undergoes release in response to microbial recognition and inflammatory signals. Released PTX3 can partially localize in neutrophil extracellular traps formed by extruded DNA. Eosinophils and basophils do not contain preformed PTX3. PTX3-deficient neutrophils have defective microbial recognition and phagocytosis, and PTX3 is nonredundant for neutrophil-mediated resistance against Aspergillus fumigatus. Thus, neutrophils serve as a reservoir, ready for rapid release, of the long PTX3, a key component of humoral innate immunity with opsonic activity.

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          Convergence of Wnt, beta-catenin, and cadherin pathways.

          W Nelson (2004)
          The specification and proper arrangements of new cell types during tissue differentiation require the coordinated regulation of gene expression and precise interactions between neighboring cells. Of the many growth factors involved in these events, Wnts are particularly interesting regulators, because a key component of their signaling pathway, beta-catenin, also functions as a component of the cadherin complex, which controls cell-cell adhesion and influences cell migration. Here, we assemble evidence of possible interrelations between Wnt and other growth factor signaling, beta-catenin functions, and cadherin-mediated adhesion.
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            The acute phase response.

            H. Baumann, J Gauldie (1994)
            Adult mammals respond to tissue damage by implementing the acute phase response, which comprises a series of specific physiological reactions. This review outlines the principal cellular and molecular mechanisms that control initiation of the tissue response at the site of injury, the recruitment of the systemic defense mechanisms, the acute phase response of the liver and the resolution of the acute phase response.
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              Pentraxins at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.

              Cecilia Garlanda, Barbara Bottazzi, Antonio Bastone … (2005)
              C reactive protein, the first innate immunity receptor identified, and serum amyloid P component are classic short pentraxins produced in the liver. Long pentraxins, including the prototype PTX3, are expressed in a variety of tissues. Some long pentraxins are expressed in the brain and some are involved in neuronal plasticity and degeneration. PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. PTX3 acts as a functional ancestor of antibodies, recognizing microbes, activating complement, and facilitating pathogen recognition by phagocytes, hence playing a nonredundant role in resistance against selected pathogens. In addition, PTX3 is essential in female fertility because it acts as a nodal point for the assembly of the cumulus oophorus hyaluronan-rich extracellular matrix. Thus, the prototypic long pentraxin PTX3 is a multifunctional soluble pattern recognition receptor at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exp Med
                Title: The Journal of Experimental Medicine
                Publisher: The Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date (Print): 16 April 2007
                Volume: 204
                Issue: 4
                Pages: 793-804
                Affiliations
                [1 ]Institut National de la Santé et de la Recherche Médicale, Equipe Avenir, Unité 564, University Hospital of Angers, University of Angers, Angers 49933, France
                [2 ]Istituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico, 20089 Rozzano, Italy
                [3 ]Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 05122 Perugia, Italy
                [4 ]Institut National de la Santé et de la Recherche Médicale, Unité 564, University of Angers, 49933 Angers, France
                [5 ]Department of Pathology, University of Verona, 37134 Verona, Italy
                [6 ]Immunology and Allergology Laboratory, University Hospital of Angers, 49933 Angers, France
                [7 ]Institute of General Pathology, Faculty of Medicine, University of Milan, 20100 Milan, Italy
                Author notes

                CORRESPONDENCE Alberto Mantovani: alberto.mantovani@ 123456humanitas.it OR Pascale Jeannin: pascale.jeannin@ 123456univ-angers.fr

                Article
                Publisher ID: 20061301
                DOI: 10.1084/jem.20061301
                PMC ID: 2118544
                PubMed ID: 17389238
                SO-VID: 63bdbcb2-66b5-49dc-bc09-bf968ceba4f7
                Copyright © Copyright © 2007, The Rockefeller University Press
                History
                Date received : 19 June 2006
                Date accepted : 15 February 2007
                Categories
                Subject: Articles
                Subject: Article

                ScienceOpen disciplines: Medicine
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                ScienceOpen disciplines: Medicine

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