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- Publisher Website: 10.4049/jimmunol.1401009
- Scopus: eid_2-s2.0-84958554883
- PMID: 26773156
- WOS: WOS:000369632300008
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Article: C1q modulates the response to TLR7 stimulation by pristane-primed macrophages: Implications for pristane-induced lupus
Title | C1q modulates the response to TLR7 stimulation by pristane-primed macrophages: Implications for pristane-induced lupus |
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Authors | |
Issue Date | 2016 |
Citation | Journal of Immunology, 2016, v. 196, n. 4, p. 1488-1494 How to Cite? |
Abstract | Copyright © 2016 by The American Association of Immunologists, Inc. The complement component C1q is known to play a controversial role in the pathogenesis of systemic lupus erythematosus, but the underlying mechanisms remain poorly understood. Intraperitoneal injection of pristane induces a lupus-like syndrome whose pathogenesis implicates the secretion of type I IFN by CD11b+ Ly6Chigh inflammatory monocytes in a TLR7-dependent fashion. C1q was also shown to influence the secretion of IFN-α. In this study, we explored whether C1q deficiency could affect pristaneinduced lupus. Surprisingly, C1qa-/- mice developed lower titers of circulating Abs and milder arthritis compared with the controls. In keeping with the clinical scores, 2 wk after pristane injection the peritoneal recruitment of CD11b+ Ly6Chigh inflammatory monocytes in C1qa-/- mice was impaired. Furthermore, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3, CCL2, CXCL1, and IL-6 when stimulated in vitro with TLR7 ligand. Replenishing C1q in vivo during the pristane-priming phase rectified this defect. Conversely, pristane-primed macrophages from C3-deficient mice did not show impaired cytokine production. These findings demonstrate that C1q deficiency impairs the TLR7-dependent chemokine production by pristane-primed peritoneal macrophages and suggest that C1q, and not C3, is involved in the handling of pristane by phagocytic cells, which is required to trigger disease in this model. |
Persistent Identifier | http://hdl.handle.net/10722/279672 |
ISSN | 2023 Impact Factor: 3.6 2023 SCImago Journal Rankings: 1.558 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Carlucci, Francesco | - |
dc.contributor.author | Ishaque, Attia | - |
dc.contributor.author | Ling, Guang Sheng | - |
dc.contributor.author | Szajna, Marta | - |
dc.contributor.author | Sandison, Ann | - |
dc.contributor.author | Donatien, Philippe | - |
dc.contributor.author | Cook, H. Terence | - |
dc.contributor.author | Botto, Marina | - |
dc.date.accessioned | 2019-11-27T08:09:44Z | - |
dc.date.available | 2019-11-27T08:09:44Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Journal of Immunology, 2016, v. 196, n. 4, p. 1488-1494 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | http://hdl.handle.net/10722/279672 | - |
dc.description.abstract | Copyright © 2016 by The American Association of Immunologists, Inc. The complement component C1q is known to play a controversial role in the pathogenesis of systemic lupus erythematosus, but the underlying mechanisms remain poorly understood. Intraperitoneal injection of pristane induces a lupus-like syndrome whose pathogenesis implicates the secretion of type I IFN by CD11b+ Ly6Chigh inflammatory monocytes in a TLR7-dependent fashion. C1q was also shown to influence the secretion of IFN-α. In this study, we explored whether C1q deficiency could affect pristaneinduced lupus. Surprisingly, C1qa-/- mice developed lower titers of circulating Abs and milder arthritis compared with the controls. In keeping with the clinical scores, 2 wk after pristane injection the peritoneal recruitment of CD11b+ Ly6Chigh inflammatory monocytes in C1qa-/- mice was impaired. Furthermore, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3, CCL2, CXCL1, and IL-6 when stimulated in vitro with TLR7 ligand. Replenishing C1q in vivo during the pristane-priming phase rectified this defect. Conversely, pristane-primed macrophages from C3-deficient mice did not show impaired cytokine production. These findings demonstrate that C1q deficiency impairs the TLR7-dependent chemokine production by pristane-primed peritoneal macrophages and suggest that C1q, and not C3, is involved in the handling of pristane by phagocytic cells, which is required to trigger disease in this model. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Immunology | - |
dc.title | C1q modulates the response to TLR7 stimulation by pristane-primed macrophages: Implications for pristane-induced lupus | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.4049/jimmunol.1401009 | - |
dc.identifier.pmid | 26773156 | - |
dc.identifier.scopus | eid_2-s2.0-84958554883 | - |
dc.identifier.volume | 196 | - |
dc.identifier.issue | 4 | - |
dc.identifier.spage | 1488 | - |
dc.identifier.epage | 1494 | - |
dc.identifier.eissn | 1550-6606 | - |
dc.identifier.isi | WOS:000369632300008 | - |
dc.identifier.issnl | 0022-1767 | - |