CD19⁺CD24^hiCD38^hi B Cell Dysfunction in Primary Biliary Cholangitis

Figure 7

CD19⁺CD24^hiCD38^hi B cells from PBC patients failed to suppress Th1 cell differentiation, but promoted Th1 cell differentiation. PBMC isolated from PBC patients or HC subjects were divided into two populations. One was stained with CD19, CD24, and CD38 mAbs and assessed by flow cytometry. The other was stimulated with phorbol ester, ionomycin, and Brefeldin A for 6 h, then surface stained with CD4 mAbs, permeabilized, and stained with IFN-γ or IL-17 mAbs and assessed by flow cytometry. (a) Graphs showing the frequency of Th1 and Th17 cells from 20 PBC patients and 20 HC subjects. (b) Correlation between CD19⁺CD24^hiCD38^hi B cell frequency and Th1 or Th17 cell frequency from PBC patients. (c, d) CD19⁺CD24^hiCD38^hi B cells from PBC patients and HC subjects were sorted by flow cytometry and then cocultured with HC subject subset CD⁺T cells for 6 D, and Th1 cell frequency was measured by flow cytometry. Representative (c) contour plots and (d) graphs showed healthy CD19⁺CD24^hiCD38^hi B cells suppressed autologous Th1 cell differentiation, while PBC CD19⁺CD24^hiCD38^hi B cells promoted HC Th1 cell differentiation. The data are representative of four separate experiments; .

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