title: Phenotype of resting and activated monocyte-derived dendritic cells grown from peripheral blood of patients with ankylosing spondylitis.
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.
authors.affiliation: Internal Medicine A, Bnai Zion Medical Center, Haifa 31048, P.O. Box 4940, Israel. gslobodin@yahoo.com
authors.forename: Gleb
authors.initials: G
authors.lastname: Slobodin
authors.forename: Aharon
authors.initials: A
authors.lastname: Kessel
authors.forename: Natalie
authors.initials: N
authors.lastname: Kofman
authors.forename: Elias
authors.initials: E
authors.lastname: Toubi
authors.forename: Itzhak
authors.initials: I
authors.lastname: Rosner
authors.forename: Majed
authors.initials: M
authors.lastname: Odeh
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D018122:B7-1 Antigen / Q000032:analysis; D051940:B7-2 Antigen / Q000032:analysis; D019013:CD40 Antigens / Q000032:analysis; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D000068800:Etanercept; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology; D007136:Immunoglobulins / Q000032:analysis; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D008875:Middle Aged; D010641:Phenotype; D018124:Receptors, Tumor Necrosis Factor; D013167:Spondylitis, Ankylosing / Q000276:immunology* / Q000473:pathology*; D000097802:CD83 Antigen
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D019013:CD40 Antigens; D000068800:Etanercept; D006684:HLA-DR Antigens; D007074:Immunoglobulin G; D007136:Immunoglobulins; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D018124:Receptors, Tumor Necrosis Factor; D000097802:CD83 Antigen