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Il-10 Induces Tgf-Β Secretion, Tgf-Β Receptor Ii Upregulation, and Iga Secretion in B Cells Publisher Pubmed



Bagheri Y1, 2, 3 ; Babaha F4 ; Falak R1, 2 ; Yazdani R3 ; Azizi G5 ; Sadri M1 ; Abolhassani H3, 6 ; Shekarabi M1, 2 ; Aghamohammadi A3
Authors
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Authors Affiliations
  1. 1. School of Medicine, Department of Immunology, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Institute of Immunology and Infectious Diseases, Immunology Research Center (IRC), Iran University of Medical Sciences, Tehran, Iran
  3. 3. Pediatrics Center of Excellence, Children’s Medical Center, Research Center for Immunodeficiencies, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Faculty of Medical Sciences, Department of Immunology, Tarbiat Modares University, Tehran, Iran
  5. 5. Non-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran
  6. 6. Department of Laboratory Medicine, Division of Clinical Immunology, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden

Source: European Cytokine Network Published:2019


Abstract

Background: Interleukin-10 (IL-10) is a pleiotropic cytokine, which has both regulatory and stimulatory effects on different immune cell types. Different studies have reported the importance of IL-10 and Transforming growth factor-beta (TGF-p) in the regulation of B cell class switching the production of immunoglobulin A (IgA); however, the underlying mechanisms remain to be fully elucidated. The objective of this study was to investigate the TGF-p response during B stimulation of human B cells by IL-10. Methods: Pan B cells of healthy donors were negatively purified by a magnetic cell separation technique. B cells were cultured with multimeric CD40 ligand (mCD40L) and IL-10 for two and seven days. After harvesting in specific days, TGF-p receptor II and surface IgA expression was determined by flow cytometry, while IgA and TGF-p secretion was assessed by enzyme-linked immunosorbent assay. Results: B cells endogenously expressed TGF-p receptor II and after 48 hours cultivation with mCD40L or mCD40L plus IL-10, both the expression of this receptor and the production of TGF-p were significantly increased. Notably, TGF-p levels following stimulation with mCD40L and IL-10 were higher than those produced by B cells stimulated with mCD40L alone. Furthermore, at day 7 and following IL-10 stimulation, there was a significant rise in the amount of IgA secretion by class-switched plasma cells, which was higher than stimulation with mCD40L alone. Conclusion: Our findings suggest that IL-10 can modulate TGF-p production and TGF-p receptor expression in mCD40-activated human B lymphocytes. © 2019, JLE/Springer.