| First Author | Deng T | Year | 2012 |
| Journal | Immunology | Volume | 135 |
| Issue | 1 | Pages | 40-50 |
| PubMed ID | 22043818 | Mgi Jnum | J:179716 |
| Mgi Id | MGI:5302925 | Doi | 10.1111/j.1365-2567.2011.03511.x |
| Citation | Deng T, et al. (2012) Toll-like receptor-mediated inhibition of Gas6 and ProS expression facilitates inflammatory cytokine production in mouse macrophages. Immunology 135(1):40-50 |
| abstractText | Activation of Toll-like receptors (TLRs) triggers rapid inflammatory cytokine production in various cell types. The exogenous product of growth-arrest-specific gene 6 (Gas6) and Protein S (ProS) inhibit the TLR-triggered inflammatory responses through the activation of Tyro3, Axl and Mer (TAM) receptors. However, regulation of the Gas6/ProS-TAM system remains largely unknown. In the current study, mouse macrophages are shown to constitutively express Gas6 and ProS, which synergistically suppress the basal and TLR-triggered production of inflammatory cytokines, including those of tumour necrosis factor-alpha, interleukin-6 and interleukin-1beta, by the macrophages in an autocrine manner. Notably, TLR signalling markedly decreases Gas6 and ProS expression in macrophages through the activation of the nuclear factor-kappaB. Further, the down-regulation of Gas6 and ProS by TLR signalling facilitates the TLR-mediated inflammatory cytokine production in mouse macrophages. These results describe a self-regulatory mechanism of TLR signalling through the suppression of Gas6 and ProS expression. |
