Background Both rheumatoid arthritis (RA) and ankylosing spondylitis (AS) belong to the group of chronic rheumatic diseases with the important role of autoimmune pathogenic mechanisms. However, these forms differ in the major target tissues as well as the intensity of bone and cartilage destruction, with RA being the prototype of “destructive” arthritis affecting peripheral joints and AS being the prototype of “remodeling” arthritis predominantly of the axial skeleton.
Objectives Both forms of arthritis are associated with abnormal immune cell functions, including B lymphocytes. Although several recent studies stressed the role of B lymphocyte subpopulations and autoantibodies in AS, these mechanisms in the AS pathogenesis are significantly less understood compared to RA and other rheumatic autoimmune diseases.The aim of our study was to compare the frequency of B lymphocyte subpopulations between RA and AS patients, and to correlate them with the disease activity.
Methods Mononuclear cells were isolated from peripheral blood of healthy controls (n=30), RA (n=33) and AS (n=18) patients, after obtaining Ethical approval and informed consent from patients. The B lymphocyte phenotype of peripheral-blood mononuclear cells was determined using flow cytometry for the following surface markers: CD19, CD27, IgD, CD32 and CD38. In addition, statistical correlation was assessed to test the association between the frequency of selected B lymphocyte subpopulations and the disease-activity score, DAS28 (Disease Activity Score 28) for RA and BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) for AS.
Results Gating strategy applied for flow-cytometry data was set to discriminate between naïve B lymphocytes (CD19+ IgD+ CD27-), unswitched memory B lymphocytes (CD19+ IgD+ CD27+), class-switched memory B lymphocytes (CD19+ IgD- CD27-) and plasmablasts (CD19+ IgD+ CD27hi CD38+). In addition, expression of CD32 (FcgRII receptor) and CD86 (B7-2 co-stimulator), associated with the maturation and activation of B lymphocytes, within these B lymphocyte subsets were assessed. Data analysis showed expanded CD32+ subset among naïve and memory B lymphocytes in RA (16.4±11.6% and 9.8±8.2%) compared to control (4.3±2.7% and 7.6±3.5%) and AS (5.6±2.6% and 5.8±1.9%). Similarly, there were more CD86+ cells among naïve and unswitched memory B lymphocytes in RA (9.0±8.2% and 18.2±8.0%) compared to control (2.8±1.3% and 11.7±5.5%) and AS (4.9±5.9% and 11.6±6.2%). Class-switched memory B lymphocytes were negatively associated with disease activity score in RA (ρ=-0.45) but positively in AS (ρ=+0.39), whereas the associations were reversed for the population of naïve B lymphocytes (ρ=+0.32 for RA and ρ=-0.38 for AS).
Conclusions Our results indicate that B lymphocyte-mediated immune response may be important for both RA and AS, but with distinct effector mechanisms. Therefore it is reasonable to suggest that B lymphocyte subpopulations may represent promising cellular targets for the therapeutic interventions in different forms of arthritis.
Acknowledgement This work was fully supported by Croatian Science Foundation (project nr. 5699).
Disclosure of Interest None declared