Immune Netw.
2024 Aug;24(4):e24. 10.4110/in.2024.24.e24.
Complement C5a Receptor Signaling in Macrophages Enhances Trained Immunity Through mTOR Pathway Activation
- Affiliations
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- 1Innovative Research and Education Center for Integrated Bioactive Materials and the Department of Bioactive Material Sciences, Jeonbuk National University, Jeonju 54896, Korea
- 2Department of Bioscience, University of Science and Technology (UST), Daejeon 34113, Korea
- 3Infectious Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea
- 4Department of Molecular Biology and The Institute for Molecular Biology and Genetics, Jeonbuk National University, Jeonju 54896, Korea
- 5Department of Medicine, College of Medicine and Medical Research Institute, Chungbuk National University, Cheongju 28644, Korea
- KMID: 2562611
- DOI: http://doi.org/10.4110/in.2024.24.e24
Abstract
- Complement C5a receptor (C5aR) signaling in immune cells has various functions, inducing inflammatory or anti-inflammatory responses based on the type of ligand present. The Co1 peptide (SFHQLPARSRPLP) has been reported to activate C5aR signaling in dendritic cells. We investigated the effect of C5aR signaling via the Co1 peptide on macrophages. In peritoneal macrophages, the interaction between C5aR and the Co1 peptide activated the mTOR pathway, resulting in the production of pro-inflammatory cytokines. Considering the close associations of mTOR signaling with IL-6 and TNF-α in macrophage training, our findings indicate that the Co1 peptide amplifies β-glucan-induced trained immunity. Overall, this research highlights a previously underappreciated aspect of C5aR signaling in trained immunity, and posits that the Co1 peptide is a potentially effective immunomodulator for enhancing trained immunity.
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