Objective: Autophagy in the immune and autoimmune diseases has been concerned more and more. We investigated the potential role of cell autophagy of B cells generating IgM in primary biliary cholangitis (PBC), and explored the relationship between the cell autophagy of hepatic stellate cells (HSCs) and hepatic fibrosis in PBC. Methods: We examined the aggregation degree of microtubule-associated protein light chain 3II (LC3II) in B cells of PBC (n = 21), health control (HC, n = 15) and disease control (DC, n = 8, active hepatitis B). The expression level of p62/SQSTM1 (p62) in B cells was detected by flow cytometry. ELISA was adopted to detect the level of IgM in the B cell culture supernatant under the basal condition, activated condition(stimulated by pokeweed mitogen, PWM) and inhibited condition(inhibited by autophagy inhibitor, 3-methyladenine, 3-MA) respectively. We detected the expression of α-smooth muscle actin (α-SMA), the infiltration level of LC3II, transforming growth factor-β (TGF-β), platelet-derived growth factor-bb (PDGF-bb), and collagen I in the hepatic tissues of five PBC patients and two HC individuals. Results: When B cells were stimulated and activated by PWM, the expression of p62 increased, and the mean fluorescence intensity (MFI, 2404.8 ± 689.0) of p62 in PBC was lower than that in HC (2966.8 ± 488.9,P = 0.0227). Under 3-MA treatment, the MFI expressed of p62 in B cells weakened. The reduction difference in PBC (466.4 ± 214.9) was smaller than that in HC (1166.6 ± 231.2, P = 0.0000) and DC (1184.8 ± 197.7, P = 0.0001). The level of generating IgM in the PBC group was obviously higher than that in the HC group (65.7 ± 15.4 vs. 49.5 ± 20.4 ng/ml, P = 0.0357). Before and after B cells were treated with 3-MA, the peak level of IgM did not significantly diminish in PBC and DC (65.7 ± 15.4 vs. 59.6 ± 18.7 ng/ml, P = 0.2965; 50.1 ± 17.4 vs. 48.4 ± 12.3 ng/ml, P = 0.8336). The immunohistochemical result revealed that the expression level of collagen I, α-SMA, TGF-β and PDGF-bb in PBC was higher than that in HC, but the expression of LC3II was lower. Similarly, immunofluorescence assay revealed that the fluorescence intensity of collagen I was higher but LC3II was lower in PBC than that in HC. Conclusion: The high level autophagy of B cells from PBC patients is one important factor to synthesize and secrete IgM. Hepatic fibrosis of PBC is probably associated with the weakened autophagy of HSCs. Key Points • High-level autophagy of B cells in PBC patients is an important factor to synthesize and secrete IgM. • Pro-fibrogenic cytokines in PBC influence the increase of collagen-I through HSC autophagy, and promote the occurrence and development of hepatic fibrosis. [ABSTRACT FROM AUTHOR]