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Title: | SLAMF5 enhances autophagy and fine-tunes cytokine response in monocyte-derived dendritic cells via stabilization of Interferon regulatory Factor 8 |
Author: | Agod, Zsofia Pazmandi, Kitti Bencze, Dóra Vereb, Gyorgy Biro, Tamas Szabo, Attila Rajnavolgyi, Eva Bacsi, Attila Engel Rocamora, Pablo Lanyi, Arpad |
Keywords: | Citoquines Autofàgia Cèl·lules dendrítiques Cytokines Autophagy Dendritic cells |
Issue Date: | 26-Jan-2018 |
Publisher: | Frontiers Media |
Abstract: | Signaling lymphocyte activation molecule family (SLAMF) receptors are essential regulators of innate and adaptive immune responses. The function of SLAMF5/CD84, a family member with almost ubiquitous expression within the hematopoietic lineage is poorly defined. In this article, we provide evidence that in human monocyte-derived dendritic cells (moDCs) SLAMF5 increases autophagy, a degradative pathway, which is highly active in dendritic cells (DCs) and plays a critical role in orchestration of the immune response. While investigating the underlying mechanism, we found that SLAMF5 inhibited proteolytic degradation of interferon regulatory factor 8 (IRF8) a master regulator of the autophagy process by a mechanism dependent on the E3-ubiquitin ligase tripartite motif-containing protein 21 (TRIM21). Furthermore, we demonstrate that SLAMF5 influences the ratio of CD1a+ cells in differentiating DCs and partakes in the regulation of IL-1β, IL-23, and IL-12 production in LPS/IFNγ-activated moDCs in a manner that is consistent with its effect on IRF8 stability. In summary, our experiments identified SLAMF5 as a novel cell surface receptor modulator of autophagy and revealed an unexpected link between the SLAMF and IRF8 signaling pathways, both implicated in multiple human pathologies. |
Note: | Reproducció del document publicat a: https://doi.org/10.3389/fimmu.2018.00062 |
It is part of: | Frontiers in Immunology, 2018, vol. 9, p. 62 |
URI: | http://hdl.handle.net/2445/146501 |
Related resource: | https://doi.org/10.3389/fimmu.2018.00062 |
ISSN: | 1664-3224 |
Appears in Collections: | Articles publicats en revistes (Biomedicina) |
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