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The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells
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| Zeitschriftentitel: | Journal of Leukocyte Biology |
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| Personen und Körperschaften: | , , , , , , |
| In: | Journal of Leukocyte Biology, 80, 2006, 1, S. 87-95 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Oxford University Press (OUP)
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| Schlagwörter: |
| author_facet |
Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia |
|---|---|
| author |
Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia |
| spellingShingle |
Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia Journal of Leukocyte Biology The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells Cell Biology Immunology Immunology and Allergy |
| author_sort |
baruah, paramita |
| spelling |
Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia 1938-3673 0741-5400 Oxford University Press (OUP) Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1189/jlb.0805445 <jats:title>Abstract</jats:title> <jats:p>Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll-like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross-presentation of the MELAN-A/melanoma antigen-reactive T cell 1 (MART-1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen-presenting cells and possibly plays a role in immune homeostasis.</jats:p> The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells Journal of Leukocyte Biology |
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| title |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_unstemmed |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_full |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_fullStr |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_full_unstemmed |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_short |
The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_sort |
the tissue pentraxin ptx3 limits c1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| topic |
Cell Biology Immunology Immunology and Allergy |
| url |
http://dx.doi.org/10.1189/jlb.0805445 |
| publishDate |
2006 |
| physical |
87-95 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll-like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross-presentation of the MELAN-A/melanoma antigen-reactive T cell 1 (MART-1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen-presenting cells and possibly plays a role in immune homeostasis.</jats:p> |
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| author_facet | Baruah, Paramita, Dumitriu, Ingrid E, Peri, Giuseppe, Russo, Vincenzo, Mantovani, Alberto, Manfredi, Angelo A, Rovere-Querini, Patrizia, Baruah, Paramita, Dumitriu, Ingrid E, Peri, Giuseppe, Russo, Vincenzo, Mantovani, Alberto, Manfredi, Angelo A, Rovere-Querini, Patrizia |
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| description | <jats:title>Abstract</jats:title> <jats:p>Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll-like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross-presentation of the MELAN-A/melanoma antigen-reactive T cell 1 (MART-1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen-presenting cells and possibly plays a role in immune homeostasis.</jats:p> |
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| spelling | Baruah, Paramita Dumitriu, Ingrid E Peri, Giuseppe Russo, Vincenzo Mantovani, Alberto Manfredi, Angelo A Rovere-Querini, Patrizia 1938-3673 0741-5400 Oxford University Press (OUP) Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1189/jlb.0805445 <jats:title>Abstract</jats:title> <jats:p>Pentraxins (PTX) and complement belong to the humoral arm of the innate immune system and have essential functions in immune defense to microbes and in scavenging cellular debris. The prototypic long PTX, PTX3, and the first component of the classical complement pathway, C1q, are innate opsonins involved in the disposal of dying cells by phagocytes. Whether the interaction between various innate opsonins impacts on their function is not fully understood. We show here that characterized Toll-like receptor (TLR) ligands elicit the production of C1q and PTX3 by immature dendritic cells (DC). Moreover, these molecules bind to dying cells with similar kinetics, although they recognize different domains on the cell membranes. PTX3 binds in the fluid phase to C1q, decreasing C1q deposition and subsequent complement activation on apoptotic cells. C1q increases the phagocytosis of apoptotic cells by DC and the release of interleukin-12 in the presence of TLR4 ligands and apoptotic cells; PTX3 inhibits both events. Moreover, PTX3 inhibited the cross-presentation of the MELAN-A/melanoma antigen-reactive T cell 1 (MART-1) tumor antigen expressed by dying cells, even in the presence of C1q. These results suggest that interaction of C1q and PTX3 influences the clearance of apoptotic cells by DC. The coordinated induction by primary, proinflammatory signals of C1q and PTX3 and their reciprocal regulation during inflammation influences the clearance of apoptotic cells by antigen-presenting cells and possibly plays a role in immune homeostasis.</jats:p> The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells Journal of Leukocyte Biology |
| spellingShingle | Baruah, Paramita, Dumitriu, Ingrid E, Peri, Giuseppe, Russo, Vincenzo, Mantovani, Alberto, Manfredi, Angelo A, Rovere-Querini, Patrizia, Journal of Leukocyte Biology, The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells, Cell Biology, Immunology, Immunology and Allergy |
| title | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_full | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_fullStr | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_full_unstemmed | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_short | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_sort | the tissue pentraxin ptx3 limits c1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| title_unstemmed | The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells |
| topic | Cell Biology, Immunology, Immunology and Allergy |
| url | http://dx.doi.org/10.1189/jlb.0805445 |