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Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

ABSTRACT: We report that the Serum Amyloid A protein, SAA1, is a novel, soluble co-factor able to promote pathogenic TH17 differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE132761 | GEO | 2019/12/05

REPOSITORIES: GEO

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Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

Project description:Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

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Project description:Macrophages are important regulators of the immune system and are critically involved in the pathophysiology of many diseases. Serum amlyoidosis is a protein misfolding disease which can follow chronic inflammatory conditions. Deposition of fibrils formed from serum amyloid A1 (SAA1) protein occurs systemically and can lead to severe or even fatal outcomes. Macrophages play a critical role in the misfolding and deposition of SAA1-derived fibrils and the role of macrophages in this context has been studied extensively. It is known that SAA1 can bind to some surface receptors on macrophages and it is taken up by the macrophages and metabolized in the lysosomes. On the other hand, the effect of SAA1 on macrophage physiology has been much less investigated so far. Therefore, we aim to investigate the effect of SAA1 on macrophage gene expression by gene microarray analysis. To this end, primary peritoneal macrophages from NMRI mice were treated with endotoxin-free recombinantly expressed full-length mSAA1 for 6 and 24 h and gene expression was analyzed.

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