Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.molimm.2011.02.006
Title: C1q regulation of dendritic cell development from monocytes with distinct cytokine production and T cell stimulation
Authors: Teh, B.K.
Yeo, J.G.
Chern, L.M.
Lu, J. 
Keywords: C1q
Complement
Dendritic cell
Monocyte
Phagocytosis
SLE
Th1
Th17
Issue Date: May-2011
Citation: Teh, B.K., Yeo, J.G., Chern, L.M., Lu, J. (2011-05). C1q regulation of dendritic cell development from monocytes with distinct cytokine production and T cell stimulation. Molecular Immunology 48 (9-10) : 1128-1138. ScholarBank@NUS Repository. https://doi.org/10.1016/j.molimm.2011.02.006
Abstract: The causative association of complement C1q deficiency with systemic lupus erythematosus (SLE), which inevitably involves the breakdown of tolerance, remains poorly explained. Its non-hepatic, macrophage and dendritic cell (DC) origin may be highly relevant. In tissues, C1q is produced by DCs and macrophages which deposits around these cells and we ask whether this pericellular form of C1q regulates DC development from monocytes. DCs cultured on immobilized C1q (C1q-DCs) show similar MHC, CD40, CD80, CD86, CD83 and CCR7 expression as normal DCs, but these cells exhibit increased phagocytosis of apoptotic cells and elevated IL-10 but reduced IL-12 and IL-23 production. Intracellularly, C1q-DCs exhibit increased ERK, p38 and p70S6 kinase activity. By mixed leukocyte reaction, C1q-DCs show reduced Th1 and Th17 induction from allogeneic CD4+ T cells. LPS and IFNγ, which cause normal DCs to induce increased CD25 expression on CD4+ T cells, attenuate C1q-DC induction of CD25. These imply that the DC pericellular C1q may induce tolerogenic properties in developing DCs. © 2011 Elsevier Ltd.
Source Title: Molecular Immunology
URI: http://scholarbank.nus.edu.sg/handle/10635/108280
ISSN: 01615890
DOI: 10.1016/j.molimm.2011.02.006
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