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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Expression Profile of the IL-17 Receptor Family on Peripheral B Lymphocytes in Rheumatoid Arthritis
Coronado González Christian Fernando1, Sifuentes Franco Sonia2, Hernández Bello Jorge3
1Programa Educativo Médico Cirujano y Partero, Centro Universitario de Ciencias de la Salud (CUCS), Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, udg.mx.
Abstract:
B cells are key contributors to the immunopathogenesis of rheumatoid arthritis (RA), yet the expression profile of interleukin-17 (IL-17) receptors on human B cells remains incompletely defined. We analyzed the surface expression of IL-17RA-IL-17RE on peripheral CD19+ B cells from 42 patients with RA and 20 healthy controls (HC) using flow cytometry. Receptor-positive cell frequency and mean fluorescence intensity (MFI) were evaluated, and disease activity was assessed using the Disease Activity Score in 28 joints based on erythrocyte sedimentation rate (DAS28-ESR). The frequency of receptor-positive B cells differed significantly among IL-17 receptor (IL-17R) family members in both RA and HC, with IL-17RD showing the highest proportion of positive cells, followed by IL-17RA, whereas IL-17RC was less frequent and IL-17RB and IL-17RE were rarely detected. The proportion of IL-17RA+ B cells was lower in RA than in HC and remained statistically significant after correction for multiple comparisons (Holm-adjusted p = 0.0126). A nominally lower frequency of IL-17RC+ B cells in RA did not remain significant after adjustment, while IL-17RD frequency was comparable between groups. No between-group differences in MFI remained significant after multiple-comparison correction. Receptor expression was not significantly associated with DAS28-ESR disease activity categories. These findings provide a descriptive characterization of the IL-17R family on peripheral B cells in RA and identify a lower frequency of IL-17RA+ B cells as the most robust between-group difference, suggesting alterations in IL-17R dynamics that may contribute to B-cell dysregulation and disease pathogenesis.
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