Maturation of dendritic cells abrogates C1q production in vivo and in vitro

Giuseppe Castellano, Andrea M. Woltman, Alma J. Nauta, Anja Roos, Leendert A. Trouw, Marc A. Seelen, Francesco Paolo Schena, Mohamed R. Daha, Cees Van Kooten*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

142 Citations (Scopus)

Abstract

Dendritic cells (DCs) and complement are essential components of the innate immune system. Immature DCs (immDCs) and mature DCs (mDCs) can migrate to lymphoid areas inducing, respectively, tolerance and immune responses. Primary deficiency of complement component C1q (C1q) leads to autoimmunity, suggesting a role in the maintenance of tolerance. In the present study, we investigated the production of C1q by immDCs, mDCs, and macrophages. We demonstrated that monocyte-derived and CD34+-derived interstitial DCs are a rich source of C1q. C1q produced by immDCs is functionally active in complement activation and binding to apoptotic cells. The production of C1q is completely down-regulated upon DC maturation in vitro. Moreover, we found that DC differentiation in the presence of interferon-α (IFN-α) accelerated DC maturation and strongly impaired overall C1q production. Finally, we demonstrated the presence, in significant numbers, of DC-SIGN +/C1q+ cells in T-cell areas of tonsils, next to DC-LAMP+ mDCs lacking C1q. We conclude from these results that immDC, a cell with tolerogenic properties, is a rich source of active C1q in vitro and in vivo, which is down-regulated on maturation. Therefore, immDCs may be considered an additional source of C1q in n humans.

Original languageEnglish
Pages (from-to)3813-3820
Number of pages8
JournalBlood
Volume103
Issue number10
DOIs
Publication statusPublished - 15 May 2004
Externally publishedYes

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