Journal
IMMUNOLOGY
Volume 135, Issue 1, Pages 40-50Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2567.2011.03511.x
Keywords
Gas6; inflammation; protein S; TAM receptors; toll-like receptor
Categories
Funding
- National Natural Science Foundation of China [30971459]
- Special Funds for Major State Basic Research Project of China [2007CB947504]
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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-a, interleukin-6 and interleukin-1 beta, 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-alpha B. 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.
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