Thus, B-cell-related molecular pathways may participate in the pathogenesis of myositis in this subset of patients
Thus, B-cell-related molecular pathways may participate in the pathogenesis of myositis in this subset of patients. Electronic supplementary material The online version of this article (doi:10.1186/s13075-014-0454-8) contains supplementary material, which is available to authorized users. Introduction Idiopathic inflammatory myopathies (IIMs), collectively named =11) or DM (=6) [29,30] or sporadic IBM (=6) [31]. LY-2584702 tosylate salt and/or anti-Ro52/anti-Ro60-positive patients compared to controls and to patients without these autoantibodies (= BAFF-R: 0.007, BCMA: 0.03 and TACI: 0.07). A local association of Rabbit polyclonal to PDCD4 receptors with B and plasma cells was confirmed by confocal microscopy. The numbers of CD138-positive and BCMA-positive cells were correlated (= 0.79; = 0.001). Expression of BDCA-2 correlated with numbers of CD138-positive cells and marginally with BCMA-positive cells (= 0.54 and 0.42, respectively; = 0.04 and 0.06, respectively). There was a borderline correlation between the numbers of positively stained TACI cells and MX-1 areas (= 0.38, = 0.08). Conclusions The expression pattern of receptors for BAFF on B and plasma cells in muscle mass suggests a local role for BAFF in autoantibody production in muscle tissues of patients with myositis who have anti-Jo-1 or anti-Ro52/anti-Ro60 autoantibodies. BAFF production could be influenced by type-I IFN produced by pDCs. Thus, B-cell-related molecular pathways may LY-2584702 tosylate salt participate in the pathogenesis of myositis in this subset of patients. Electronic supplementary material The online version of this article (doi:10.1186/s13075-014-0454-8) contains supplementary material, which is available to authorized users. LY-2584702 tosylate salt Introduction Idiopathic inflammatory myopathies (IIMs), collectively named =11) or DM (=6) [29,30] or sporadic IBM (=6) [31]. They have been reported previously [23]. The median duration from diagnosis until the time of muscle mass biopsy was 0.5?years (minumum – maximum range: 0 to 22.5?years), and mean age (SD) was 56.1??12.3?years. At the time of biopsy, 19 patients were being treated with immunosuppressive brokers, and the median period of treatment was 1.6?years (range, 0 to 28.5) (Table?1). Three patients with IBM (patients 10, 17 and 23) (Table?1) formerly diagnosed with PM were treated before the diagnosis of IBM was made (13.7, 9 and 3.2?years, respectively). Biopsy specimens from seven healthy individuals (four women and three men; mean age (SD) =60.7??13.6?years) were included as controls. All patients and control individuals gave their informed consent to participate, and the local ethics committee at the Karolinska Hospital Nord, Stockholm, approved the study. Table 1 Clinical characteristics and autoantibody profiles of patients at time of muscle mass biopsy a and results of immunohistochemical analysis of biopsies =23) [23]. Evaluation of immunohistochemical staining Entire tissue sections were analysed using a standard microscope (Reichert-Jung Polyvar 2; Leica, Vienna, Austria) in a coded manner by three impartial assessors. The mean numbers of cells positive for receptors for BAFF, CD19 and CD138 per square millimetre of muscle tissue were calculated. The number of cells positive for staining for receptors was tested for a possible correlation with the expression of pDC marker BDCA-2/CD303 and MX-1 protein in consecutive serial sections, expressed as the percentage of positively stained area per total tissue section (Table?2). A quantitative evaluation of BDCA-2 and MX-1 protein expression was performed by computerised image analysis on the total tissue area using the Leica QWin software and microscope (DM RXA2; Leica, Wetzlar, Germany). There was a high degree of correlation between the results of standard microscopic evaluation and those of computerised image analysis of BDCA-2-positive cells and of total MX-1 expression, as previously reported [23]. Table 2 Correlations between expression of receptors for BAFF and expression of markers for B and plasma cells, type I IFN production and plasmacytoid dendritic cells.