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Additional file 3: Table S1. Clinical, biological and pathological characteristics of patients with IgG4-RD and HCs. Baseline caharacteristics of patients with IgG4-RD (n = 21) and HC (n = 10) are shown. PSL: prednisolone. (PDF format)

Additional file 3: Table S1. Clinical, biological and pathological characteristics of patients with IgG4-RD and HCs. Baseline caharacteristics of patients with IgG4-RD (n = 21) and HC (n = 10) are shown. PSL: prednisolone. (PDF format)

Additional file 1: Figure S1. Expression of IL-21 and IL-10 mRNA in SLAMF7+ activated Tfh1 cells and activated Tfh2 cells in IgG4-RD. Comparison of levels of IL-21 and IL-10 mRNA in SLAMF7+PD-1+ Tfh1 cells and PD-1+ Tfh2 cells in the peripheral blood of patients with IgG4-RD (n = 5). * indicates p

Additional file 2: Figure S2. Expression of Ascl2 mRNA and CXCR5 protein in Tfh1 subsets in patients with IgG4-RD. (A) Comparison of levels of Ascl2 mRNA in PD-1− Tfh1 cells, SLAMF7−PD-1+ Tfh1 cells and SLAMF7+PD-1+ Tfh1 cells in the peripheral blood of patients with IgG4-RD (n = 8). (B) Comparison of surface CXCR5 expression in PD-1− Tfh1 cells, SLAMF7−PD-1+ Tfh1 cells and SLAMF7+PD-1+ Tfh1 cells in IgG4-RD patients (shadow: isotype control; dotted line: SLAMF7+PD-1+Tfh1 cells; solid line: SLAMF7−PD-1+Tfh1 cells). * indicates p

Additional file 2: Figure S2. Expression of Ascl2 mRNA and CXCR5 protein in Tfh1 subsets in patients with IgG4-RD. (A) Comparison of levels of Ascl2 mRNA in PD-1− Tfh1 cells, SLAMF7−PD-1+ Tfh1 cells and SLAMF7+PD-1+ Tfh1 cells in the peripheral blood of patients with IgG4-RD (n = 8). (B) Comparison of surface CXCR5 expression in PD-1− Tfh1 cells, SLAMF7−PD-1+ Tfh1 cells and SLAMF7+PD-1+ Tfh1 cells in IgG4-RD patients (shadow: isotype control; dotted line: SLAMF7+PD-1+Tfh1 cells; solid line: SLAMF7−PD-1+Tfh1 cells). * indicates p

Table S1. List of antibodies used in flow cytometry (DOCX 23 kb)

Figure S1. Change in lymphocyte reconstitution over a 5-year period. Figure S2. Changes in skin sclerosis and pulmonary function over an 8-year period. (PDF 348 kb)

Table S2. Clinical characteristics of patients with RA. TCZ, Tocilizumab. ETN, Etanercept. MZR, Mizoribine. IGU, Iguratimod. (DOCX 16 kb)

Clinical characterization of patients with RA included in the study. (DOCX 18 kb)

Analysis of osteoclast differentiation using RAW-Venus1. (A) Differentiation into Venus positive pre-osteoclasts and osteoclasts were induced by RANKL in a dose-dependent manner. TNF-α exerted synergistic effects on RANKL-induced osteoclast differentiation (magnification × 20). (B) Both anti-RANKL Ab and OPG strongly reduced the number of Venus positive cells, indicated the inhibition of osteoclast differentiation (magnification × 20). (C) Venus positive cells were tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (magnification × 40). Cells were stained using a commercial TRAP assay (Sigma-Aldrich, St Louis, MO, USA). (A-C) Cells were cultured at 4.5 × 104 cells/ml for 3 days in a 96-well plate. No stim No stimulation. (PDF 304 kb)

Phenotypic analysis of RANKL+ and RANKL− effector memory B cells. Purified switched-memory B cells from HC were stimulated with BCR/CD40 and IFN-γ for 48 hours. RANKL+ and RANKL− cells were analyzed for expression of CD20, CD21, CD95, CD11c, CCR1 and CCR5 using respective Abs (all from BioLegend). Representative data are shown (n = 3–4). (PDF 177 kb)

Clinical characterization of patients with RA included in the study. (DOCX 18 kb)

Analysis of osteoclast differentiation using RAW-Venus1. (A) Differentiation into Venus positive pre-osteoclasts and osteoclasts were induced by RANKL in a dose-dependent manner. TNF-α exerted synergistic effects on RANKL-induced osteoclast differentiation (magnification × 20). (B) Both anti-RANKL Ab and OPG strongly reduced the number of Venus positive cells, indicated the inhibition of osteoclast differentiation (magnification × 20). (C) Venus positive cells were tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (magnification × 40). Cells were stained using a commercial TRAP assay (Sigma-Aldrich, St Louis, MO, USA). (A-C) Cells were cultured at 4.5 × 104 cells/ml for 3 days in a 96-well plate. No stim No stimulation. (PDF 304 kb)

Phenotypic analysis of RANKL+ and RANKL− effector memory B cells. Purified switched-memory B cells from HC were stimulated with BCR/CD40 and IFN-γ for 48 hours. RANKL+ and RANKL− cells were analyzed for expression of CD20, CD21, CD95, CD11c, CCR1 and CCR5 using respective Abs (all from BioLegend). Representative data are shown (n = 3–4). (PDF 177 kb)