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https://hdl.handle.net/10316/109220
Title: | Sera from patients with active systemic lupus erythematosus patients enhance the toll-like receptor 4 response in monocyte subsets | Authors: | Carvalheiro, Tiago Gomes, Diane Pinto, Ligia A Inês, Luís Lopes, Ana Henriques, Ana Pedreiro, Susana Martinho, António Trindade, Hélder Young, Howard A Silva, José António Pereira da Paiva, Artur |
Keywords: | Systemic lupus erythematosus; Serum; Cytokines; Toll like receptor 4; Classical monocytes; Non-classical monocytes; Myeloid dendritic cells | Issue Date: | 2015 | Publisher: | Springer Nature | Project: | Portuguese Society of Rheumatology (SPR): “Bolsa de Investigação na área das Doenças Reumáticas Inflamatórias – Bolsa SPR/MSD 2014” Intramural Research Program of the NIH, National Cancer Institute |
Serial title, monograph or event: | Journal of Inflammation (United Kingdom) | Volume: | 12 | Issue: | 1 | Abstract: | Background: Systemic Lupus Erythematosus (SLE) is an auto-immune disease whose complex pathogenesis remains unraveled. Here we aim to explore the inflammatory ability of SLE patients’ sera upon peripheral blood (PB) monocyte subsets and myeloid dendritic cells (mDCs) obtained from healthy donors. Methods: In this study we included 11 SLE patients with active disease (ASLE), 11 with inactive disease (ISLE) and 10 healthy controls (HC). PB from healthy donors was stimulated with patients’ sera, toll-like receptor (TLR) 4 ligand – lipopolysaccharide or both. The intracellular production of TNF-α was evaluated in classical, non-classical monocytes and mDCs, using flow cytometry. TNF-α mRNA expression was assessed in all these purified cells, after sera treatment. Results: We found that sera of SLE patients did not change spontaneous TNF-α production by monocytes or dendritic cells. However, upon stimulation of TLR4, the presence of sera from ASLE patients, but not ISLE, significantly increased the intracellular expression of TNF-α in classical and non-classical monocytes. This ability was related to titers anti-double stranded DNA antibodies in the serum. High levels of anti-TNF-α in the patients’ sera were associated with increased TNF-α expression by co-cultured mDCs. No relationship was found with the levels of a wide variety of other pro-inflammatory cytokines. A slight increase of TNF-α mRNA expression was observed in these purified cells when they were cultured only in the presence of SLE serum. Conclusions: Our data suggest that SLE sera induce an abnormal in vitro TLR4 response in classical and non-classical monocytes, reflected by a higher TNF-α intracellular expression. These effects may be operative in the pathogenesis of SLE. | URI: | https://hdl.handle.net/10316/109220 | ISSN: | 1476-9255 | DOI: | 10.1186/s12950-015-0083-2 | Rights: | openAccess |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
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