Detail Butyrate Conditions Human Dendritic Cells to Prime Type 1 Regulatory T Cells via both Histone Deacetylase Inhibition and G Protein-Coupled Receptor 109A Signaling (article of Frontiers in Immunology 2017 Oct 30; 8:1429) Bibliografi Author: Kaisar, Maria Mardalena Martini ; Pelgrom, Leonard R. ; Alwin J van der Ham ; Yazdanbakhsh, Maria ; Everts, Bart Topik: G-coupled protein receptor 109A; butyrate; dendritic cells; histone deacetylases; retinaldehyde dehydrogenase; retinoic acid; short-chain fatty acids; type 1 regulatory T cells; JABFUNG-FKIK-MKS-2022-04 Bahasa: (EN )     Penerbit: Frontiers Media S.A.     Tahun Terbit: 2017     Jenis: Article - diterbitkan di jurnal ilmiah internasional Fulltext: B4 Publikasi bu Maria Kaisar.pdf (2.11MB; 1 download) [Informasi yang berkaitan dengan koleksi ini di internet] Abstract Recently, it has become clear that short-chain fatty acids (SCFAs), and in particular butyrate, have anti-inflammatory properties. Murine studies have shown that butyrate can promote regulatory T cells via the induction of tolerogenic dendritic cells (DCs). However, the effects of SCFAs on human DCs and how they affect their capacity to prime and polarize T-cell responses have not been addressed. Here, we report that butyrate suppresses LPS-induced maturation and metabolic reprogramming of human monocyte-derived DCs (moDCs) and conditions them to polarize naive CD4+ T cells toward IL-10-producing type 1 regulatory T cells (Tr1). This effect was dependent on induction of the retinoic acid-producing enzyme retinaldehyde dehydrogenase 1 in DCs. The induction of retinaldehyde dehydrogenase activity and Tr1 cell differentiation by butyrate was dependent on simultaneous inhibition of histone deacetylases and signaling through G protein-coupled receptor 109A. Taken together, we reveal that butyrate is a potent inducer of tolerogenic human DCs, thereby shedding new light on the cellular and molecular mechanisms through which SCFAs can exert their immunomodulatory effects in humans. Opini Anda Klik untuk menuliskan opini Anda tentang koleksi ini! Lihat Sejarah Pengadaan  Konversi Metadata   Kembali

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