| First Author | Sutavani RV | Year | 2018 |
| Journal | J Biol Chem | Volume | 293 |
| Issue | 7 | Pages | 2302-2317 |
| PubMed ID | 29229781 | Mgi Jnum | J:258440 |
| Mgi Id | MGI:6117663 | Doi | 10.1074/jbc.M117.805424 |
| Citation | Sutavani RV, et al. (2018) Differential control of Toll-like receptor 4-induced interleukin-10 induction in macrophages and B cells reveals a role for p90 ribosomal S6 kinases. J Biol Chem 293(7):2302-2317 |
| abstractText | Increasing evidence has linked dysregulated interleukin (IL)-10 production by IL-10(+ve) B cells to autoimmunity, highlighting the importance of improving the understanding of the regulation of IL-10 production in these cells. In both B cells and myeloid cells, IL-10 can be produced in response to Toll-like receptor (TLR) agonists. In macrophages, previous studies have established that mitogen- and stress-activated protein kinases (MSKs) regulate IL-10 production via the phosphorylation of cAMP response element-binding (CREB) protein on the IL-10 promoter. We found here that although MSKs are activated in peritoneal B cells in response to TLR4 agonists, neither MSKs nor CREB are required for IL-10 production in these cells. Using a combination of chemical inhibitors and knockout mice, we found that IL-10 induction in B cells was regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism, unlike in macrophages in which p90 ribosomal S6 kinase was not required. This observation highlights fundamental differences in the signaling controlling IL-10 production in B cells and macrophages, even though these two cell types respond to a common TLR stimulus. |
