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CD19+CD24hiCD38hi B Cell Dysfunction in Primary Biliary Cholangitis
Qubo Chen1, Lanmin Lai1, Xiaoling Chi2
1Biological Resource Center, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, 510120 Guangzhou, China.
Mediators of Inflammation
|February 28, 2020
Summary
Patients with primary biliary cholangitis (PBC) have increased transitional B cells (CD19+CD24hiCD38hi), but these cells are functionally impaired. This immune dysfunction in PBC patients may contribute to disease progression.
Area of Science:
- Immunology
- Autoimmune Diseases
- B cell biology
Background:
- Transitional B cells (CD19+CD24hiCD38hi) normally suppress immunity via IL-10.
- These cells are altered in autoimmune diseases.
- The role of these B cells in primary biliary cholangitis (PBC) was previously unknown.
Purpose of the Study:
- To investigate the frequency and function of circulating CD19+CD24hiCD38hi B cells in PBC patients.
- To determine if these cells correlate with disease parameters.
- To assess their impact on T cell differentiation.
Main Methods:
- Flow cytometry to quantify CD19+CD24hiCD38hi B cells in peripheral blood.
- Analysis of cytokine (IL-10, TNF-α, IL-6, IL-12) and Tim-1 levels in these B cells.
- Coculture experiments to evaluate effects on CD4+ T cell differentiation.
Main Results:
- PBC patients showed a higher percentage of CD19+CD24hiCD38hi B cells, correlated with cholestasis.
- Activated B cells from PBC patients produced less IL-10 and more IL-6 and IL-12.
- Tim-1 levels were downregulated, and these B cells showed reduced T cell inhibition and promoted Th1 differentiation.
Conclusions:
- PBC patients exhibit expanded but functionally impaired CD19+CD24hiCD38hi B cells.
- These cells display a proinflammatory profile and reduced immune suppressive capacity.
- This altered B cell subset may contribute to the pathogenesis of PBC.
