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Originally published online as doi:10.1189/jlb.0805445 on April 14, 2006

Published online before print April 14, 2006
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(Journal of Leukocyte Biology. 2006;80:87-95.)
© 2006 by Society for Leukocyte Biology

The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells

Paramita Baruah*, Ingrid E. Dumitriu*, Giuseppe Peri{dagger}, Vincenzo Russo{ddagger}, Alberto Mantovani{dagger},§, Angelo A. Manfredi*,¶ and Patrizia Rovere-Querini*,1

* Clinical Immunology Unit and
{ddagger} Cancer Gene Therapy Unit, Cancer Immunotherapy & Gene Therapy Program, H. San Raffaele Scientific Institute, Milano, Italy;
{dagger} Istituto Clinico Humanitas, Rozzano, Italy;
§ Centro di Eccellenza per l’Innovazione Diagnostica e Terapeutica (IDET), Institute of General Pathology, University of Milan, Italy; and
Vita-Salute San Raffaele University, Milano, Italy

1 Correspondence: Cancer Immunotherapy & Gene Therapy Program, Clinical Immunology Unit, H. San Raffaele Scientific Institute, via Olgettina 58, Milano 20132, Italy. E-mail: rovere.patrizia{at}hsr.it

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.

Key Words: Toll-like receptor • systemic lupus erythematosus • lipopolysaccharide • apoptosis • inflammation




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