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Toll-like Receptor-2 Expression Is Upregulated in Antigen-Presenting Cells from Patients with Psoriatic Arthritis: A Pathogenic Role for Innate Immunity?
LILIANA CANDIA, JAVIER MARQUEZ, CLAUDIA HERNANDEZ, ARNOLD H. ZEA, and LUIS R. ESPINOZA ABSTRACT. 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-a (TNF-a), interferon-g (IFN-g), 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-a, IFN-g, 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. (First Release Dec 15 2006; J Rheumatol 2007;34:374–9) Key Indexing Terms:
TOLL-LIKE RECEPTORS From the Section of Rheumatology, Department of Medicine, and the Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA. L. Candia, MD, Postdoctoral Fellow; J. Marquez, MD, Postdoctoral Fellow; C. Hernandez, BS, Researcher; A.H. Zea, PhD, Assistant Professor; L.R. Espinoza, MD, Professor and Chief, Rheumatology Section. Address reprint requests to Dr. L.R. Espinoza, LSU Health Sciences Center, 1542 Tulane Avenue, New Orleans, LA 70112-2822. E-mail: luisrolan@msn.com Accepted for publication August 29, 2006.
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