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Toll-Like Receptor 2 Release by Macrophages: An Anti-inflammatory Program Induced by Glucocorticoids and Lipopolysaccharide.

Front Immunol. 2019; 
Hoppst?dter J, Dembek A, Linnenberger R, Dahlem C, Barghash A, Fecher-Trost C, Fuhrmann G, Koch M, Kraegeloh A, Huwer H, Kiemer AK.
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Biochemicals … Taq polymerase (5 U/μL, #E00007), Taq buffer (#B0005), and the dNTP mix (#D0056) were from Genscript. Other chemicals were obtained from either Sigma-Aldrich or Carl Roth unless stated otherwise. Cell Culture. Cell Lines … Get A Quote

摘要

Glucocorticoids (GCs) are widely prescribed therapeutics for the treatment of inflammatory diseases, and endogenous GCs play a key role in immune regulation. Toll-like receptors (TLRs) enable innate immune cells, such as macrophages, to recognize a wide variety of microbial ligands, thereby promoting inflammation. The interaction of GCs with macrophages in the immunosuppressive resolution phase upon prolonged TLR activation is widely unknown. Treatment of human alveolar macrophages (AMs) with the synthetic GC dexamethasone (Dex) did not alter the expression of TLRs -1, -4, and -6. In contrast, TLR2 was upregulated in a GC receptor-dependent manner, as shown by Western blot and qPCR. Furthermore, long-term lipop... More

關鍵詞

corticosteroid; exosome; innate immunity; microvesicle; pulmonary macrophage
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