Format

Send to

Choose Destination
Mol Immunol. 2014 Dec;62(2):266-76. doi: 10.1016/j.molimm.2014.05.018. Epub 2014 Jun 23.

IL-10 production by B cells is differentially regulated by immune-mediated and infectious stimuli and requires p38 activation.

Author information

1
Department of Medical and Biological Sciences, University of Udine, P.le M. Kolbe, 4, 33100 Udine, Italy.
2
Department of Medical and Biological Sciences, University of Udine, P.le M. Kolbe, 4, 33100 Udine, Italy. Electronic address: carlo.pucillo@uniud.it.

Erratum in

  • Mol Immunol. 2015 Jan;99(1):606.

Abstract

IL-10 is an immune suppressive cytokine with pleiotropic effects on B cell biology. IL-10 production has a pivotal role for the regulatory suppressive functions that B cells exert in many physiological and pathological settings. Several exogenous stimuli and endogenous immune mediators can trigger IL-10-producing B cell maturation. To clarify and gain a better insight into the mechanisms of IL-10 production by B cells, we first compared the effects of LPS, CpG, agonistic CD40 mAb and BAFF on IL-10 production, and then we investigated the signal transduction mechanisms responsible for these responses. While infectious/danger stimuli determine the rapid production and release of IL-10 by B cells, a limited subset of CD40-poised, IL-10-competent B cells produce IL-10 in response to a later antigenic or infectious signal. Although BAFF is able to induce a similar subset of IL-10-competent B cells, these cells do not similarly respond to the same antigenic or infectious signals. Importantly, by using specific inhibitors of the MAP kinase pathways, we found that while il-10 gene expression triggered by the TLR agonists LPS and CpG is strongly dependent on p38 activity, the induction of IL-10 competence in CD40-activated B cells does not depend on ERK1/2, p38 or JNK pathways.

KEYWORDS:

B cells; CD40; IL-10; MyD88; TLR; p38

PMID:
24970737
DOI:
10.1016/j.molimm.2014.05.018
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center