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Pro-inflammatory cellular immune response in Behçet's disease

Date
2007
Author
Guel, Ahmet
Saruhan-Direskeneli, Güher
KANEKO, Fumio
Tugal-Tutkun, Ilknur
YENTUER, Sibel Penbe
KULABER, Ayla
AKMAN-DEMIR, Guelsen
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Abstract
Several proteins are investigated as candidate auto-antigens in the pathogenesis of Behçet's disease (BD). This study aimed to screen the cellular responses to auto-antigen (αB-crystallin, αBC), and microorganism (Streptococcus sangius KTH-1 BES-1 protein) derived peptides as well as to isopentenyl pyrophosphate (IPP). Peripheral blood mononuclear cells (PBMC) from 22 BD patients and 22 healthy controls (HC) were stimulated in vitro with αBC, BES-1 peptides, IPP and PPD and induced proliferation as well as the secreted interleukin (IL)-12 and interferon (IFN)-γ production levels were measured. We did not observe any significant difference in cellular proliferation between BD patients and HC. Induction of IL-12 secretion with αBC was stronger in BD patients (P = 0.04) and in the disease subgroup with uveitis (P = 0.027) compared the HC. When responses to PPD were compared, proliferation of PMBC was lower (P = 0.03), whereas IL-12 secretion was higher in BD (P = 0.04) as well as in patients under colchicum treatment (P = 0.04) and with vascular involvement (P = 0.006) compared to HC. BES-1373-385 peptide induced also higher IL-12 productions by PBMC of BD patients (P = 0.017) and of patients with uveitis (P = 0.013). Finally, IPP stimulated higher IL-12 secretions from PBMC in BD patients (P = 0.035) and in patients with (P = 0.02) or without (P = 0.017) uveitis or arthritis (P = 0.04), under colchicum treatment (P = 0.01) or not receiving any immunosuppressive treatment (P = 0.007) compared to HC. These results suggest a more prominent pro-inflammatory cytokine secretion from PBMC in BD patients compared to HC in response to various antigens including αBC protein, BES-1373-385, IPP and PPD. © 2007 Springer-Verlag.
URI
http://hdl.handle.net/20.500.12627/62172
https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=34548514197&origin=inward
https://doi.org/10.1007/s00296-007-0367-9
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Creative Commons Lisansı

İstanbul Üniversitesi Akademik Arşiv Sistemi (ilgili içerikte aksi belirtilmediği sürece) Creative Commons Alıntı-GayriTicari-Türetilemez 4.0 Uluslararası Lisansı ile lisanslanmıştır.

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