| First Author | Caruso R | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 15 | Pages | 3512-9 |
| PubMed ID | 19129540 | Mgi Jnum | J:148302 |
| Mgi Id | MGI:3844203 | Doi | 10.1182/blood-2008-08-172767 |
| Citation | Caruso R, et al. (2009) Inhibition of monocyte-derived inflammatory cytokines by IL-25 occurs via p38 Map kinase-dependent induction of Socs-3. Blood 113(15):3512-9 |
| abstractText | IL-25, a member of the IL-17 cytokine family, is known to enhance Th2-like responses associated with increased serum levels of IgE, IgG1, IgA, blood eosinophilia, and eosinophilic infiltrates in various tissues. However, IL-25 also abrogates inflammatory responses driven by Th17 cells. However, the cell types that respond to IL-25 and the mechanisms by which IL-25 differentially regulates immune reactions are not well explored. To identify potential targets of IL-25, we initially examined IL-25 receptor (IL-25R) in human peripheral blood cells. IL-25R was predominantly expressed by CD14(+) cells. We next assessed the functional role of IL-25 in modulating the response of CD14(+) cells to various inflammatory signals. CD14(+) cells responded to IL-25 by down-regulating the synthesis of inflammatory cytokines induced by toll-like receptor (TLR) ligands and inflammatory cytokines. Inhibition of cytokine response by IL-25 occurred via a p38 Map kinase-driven Socs-3-dependent mechanism. In vivo, IL-25 inhibited monocyte-derived cytokines and protected against LPS-induced lethal endotoxemia in mice. These data indicate that IL-25 is a negative regulator of monocyte proinflammatory cytokine responses, which may have therapeutic implications. |
