Phenotype of Resting and Activated Monocyte-Derived Dendritic Cells Grown from Peripheral Blood of Patients with Ankylosing Spondylitis |
| |
Authors: | Gleb Slobodin Aharon Kessel Natalie Kofman Elias Toubi Itzhak Rosner Majed Odeh |
| |
Institution: | (1) Internal Medicine A, Bnai Zion Medical Center, Haifa, 31048, P.O. Box 4940, Israel;(2) Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel;(3) Immunology, Bnai Zion Medical Center, Haifa, Israel;(4) Rheumatology, Bnai Zion Medical Center, Haifa, Israel |
| |
Abstract: | Decreased levels of class II major histocompatibility complex (MHC) expression and impaired formation of immunological synapse
by dendritic cells (DCs) of HLA-B27 transgenic rats have been recently demonstrated. The resulting dysfunction of DCs may
be implicated in the pathogenesis of the HLA-B27-related disease in transgenic animals. The phenotype of DCs in patients with
ankylosing spondylitis (AS) has not been evaluated. Monocyte-derived DCs (MDDCs) were grown from patients with active AS and
age-matched healthy volunteers. Surface expression of HLA-DR, co-stimulation molecules CD80, CD86 and CD40, as well as CD83
was assessed by flow cytometry and compared between the groups under 3 conditions: in resting state, after stimulation by
lipopolysaccharide (LPS) and after stimulation by LPS in the presence of etanercept, a soluble receptor of tumor necrosis
factor α. Lower baseline expression of class II MHC molecules (HLA-DR) was observed by MDDCs grown from AS patients, as compared
to healthy subjects. Post-stimulated levels of HLA-DR were comparable in both groups, suggesting greater up-regulation of
class II MHC molecules by MDDCs from AS in response to LPS. No difference between groups in the levels of expression of co-stimulation
molecules and CD83 was observed. Lower basic expression of class II MHC by the MDDCs grown from patients with AS may be associated
with impaired regulation of their activity. Functional studies on DCs from patients with AS are needed to evaluate the integrity
of their antigen-presenting function. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|