Toll-like receptor-2 expression is upregulated in antigen-presenting cells from patients with psoriatic arthritis: a pathogenic role for innate immunity?

• Published in: Journal of rheumatology Vol. 34; no. 2; pp. 374 - 379
• Main Authors: CANDIA, Liliana, MARQUEZ, Javier, HERNANDEZ, Claudia, ZEA, Arnold H, ESPINOZA, Luis R
• Format: Journal Article
• Language: English
• Published: Toronto, ON The Journal of Rheumatology 01-02-2007; Journal of Rheumatology Publishing
• Subjects: Adult; Antigen-Presenting Cells - immunology; Antigen-Presenting Cells - metabolism; Arthritis, Psoriatic - diagnosis; Arthritis, Psoriatic - immunology; Arthritis, Psoriatic - metabolism; Biological and medical sciences; Blotting, Western; Cells, Cultured; Cytokines - metabolism; Dendritic Cells - metabolism; Dermatology; Diseases of the osteoarticular system; Female; Flow Cytometry; Humans; Immunity, Innate - immunology; Inflammatory joint diseases; Leukocytes, Mononuclear - metabolism; Male; Medical sciences; Middle Aged; Psoriasis. Parapsoriasis. Lichen; Severity of Illness Index; Toll-Like Receptor 2 - metabolism; Toll-Like Receptor 4 - metabolism; Up-Regulation; Flow cytometry; Skin disease; Pathogenesis; Diseases of the osteoarticular system; Autoimmune disease; Natural immunity; Toll like receptor; Inflammatory joint disease; Cerebrospinal fluid; Spondylarthropathy; Pathogenic; Immunoblotting assay; Bacteria; Tumor; Human; Immunopathology; Dendritic cell; TOLL-LIKE RECEPTORS DENDRITIC CELLS BACTERIA RHEUMATOID ARTHRITIS PATHOGENESIS INNATE IMMUNITY; Psoriasis; Cytokine; Accessory cell; Gene expression; Psoriatic arthritis; Chronic; Rheumatoid arthritis; Toll-like receptor-2; Interferon; Toll-like receptor-4
• ISSN: 0315-162X; 1499-2752

OBJECTIVE: To study Toll-like receptor-2 (TLR-2) and TLR-4 expression in antigen-presenting cells from patients with psoriatic
arthritis (PsA). METHODS: We measured expression of TLR-2 and TLR-4 in monocyte-derived dendritic cells from patients with
PsA and with rheumatoid arthritis (RA), and in healthy controls. Dendritic cells were obtained from freshly isolated monocytes,
stimulated with granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin 4 (IL-4) after 6 days in culture.
To obtain mature dendritic cells, lipopolysaccharide stimulation and 2 additional days in culture were necessary. The expression
of TLR-2, TLR-4, HLA-DR, and CD86 was studied at baseline, at 6 days, and at 8 days by flow cytometry. To establish the functional
properties of TLR expression we studied the following cytokines in cell supernatants: tumor necrosis factor-alpha (TNF-alpha),
interferon-gamma (IFN-gamma), IL-2, IL-4, IL-5, IL-10, IL-12, IL-13, and GM-CSF. TLR-2 expression was confirmed by Western
blot analysis. RESULTS: Ten PsA patients with active disease and 8 healthy controls were studied, along with 4 patients with
RA. TLR-2 expression was increased in immature dendritic cells from patients with PsA. Monocytes and mature dendritic cells
did not show statistically significant differences. No difference was observed in the expression of TLR-4 in any cell type.
The supernatant expression of cytokines showed a Th1 pattern, mostly with increased expression of TNF-alpha, IFN-gamma, and
IL-2. Western blot analysis confirmed the increased expression of TLR-2. CONCLUSION: Upregulation of TLR-2 expression provides
support for a role of the innate immune system in the pathogenesis of PsA.