@Article{ecn.2019.0434,
AUTHOR = {Yasser Bagheri, Fateme Babaha, Reza Falak, Reza Yazdani, Gholamreza Azizi, Maryam Sadri, Hassan Abolhassani, Mehdi Shekarabi, Asghar Aghamohammadi},
TITLE = {IL-10 induces TGF-β secretion, TGF-β receptor II upregulation, and IgA secretion in B cells},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {3},
PAGES = {107--113},
URL = {http://www.techscience.com/ECN/v30n3/65392},
ISSN = {1952-4005},
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-β) 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-β 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-β receptor II and surface IgA
expression was determined by flow cytometry, while IgA and TGF-β secretion was assessed by enzyme-linked
immunosorbent assay. Results: B cells endogenously expressed TGF-β 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-β were significantly
increased. Notably, TGF-β 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-β production and TGF-β receptor expression in
mCD40-activated human B lymphocytes.},
DOI = {10.1684/ ecn.2019.0434}
}