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Complement anaphylatoxin receptors (C3aR and C5aR1) are prototypical G protein-coupled receptors (GPCRs) playing crucial physiological roles in innate immunity by combating pathogenic infections and orchestrating inflammatory responses. They continue to be important therapeutic targets for multiple disorders including autoimmune diseases, acute and chronic inflammation, and allergy-related conditions. Recent structural coverage has provided important insights into their activation and signaling, however, confounding observations in the literature related to ligand efficacy and functional responses, especially in different model systems, present a major challenge for drug discovery efforts. Here, we systematically and comprehensively profile a broad set of natural and synthetic ligands at C3aR and C5aR1 and discover a previously unanticipated level of functional specialization in terms of species-specific pharmacology and receptor activation. Taking a lead from this, we determine seventeen cryo-EM structures of different ligand-receptor-G-protein complexes and uncover distinct orientation of agonists between the human and mouse receptors despite an overlapping positioning in the orthosteric binding pocket. Combined with extensive mutagenesis and functional assays, these structural snapshots allow us to decode and validate a convergent molecular mechanism involving a "Five-Point-Switch" in these receptors that orchestrates the recognition and efficacy of diverse agonists. We also identify species-specific differences at the level of phosphorylation patterns encoded in the carboxyl-terminus of these receptors and directly visualize their impact on βarr binding and activation using cryo-EM structures. Interestingly, we observe that βarrs engage with the mouse C5aR1 using a variation of previously discovered P-X-P-P phosphorylation motif via a "Sliding-Mechanism" and also exhibit distinct oligomeric state for the human vs. mouse receptors. Taken together, this study elucidates functional specialization at the complement anaphylatoxin receptors and underlying molecular mechanisms, offering a previously lacking framework with direct and immediate implications for the development of novel therapeutics.
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http://dx.doi.org/10.1101/2025.05.26.656101 | DOI Listing |
Immune Netw
August 2025
Center for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for Prevention of Human Diseases, UTHealth-McGovern Medical School, Houston, TX 77030, USA.
Complement anaphylatoxins C3a and C5a are potent immunomodulators whose impact extends well beyond their traditional roles in innate immunity. Acting through G protein-coupled receptors C3aR, C5aR1, and C5aR2, these peptides take part in coordinating immune cell recruitment, vascular tone, and tissue remodeling. Yet their functions are deeply context-dependent: while they play essential roles in microbial clearance and immune coordination, their overactivation contributes to immunopathology in a wide range of diseases.
View Article and Find Full Text PDFBiochim Biophys Acta Rev Cancer
September 2025
Department of Neurosurgery, The First Hospital of China Medical University, Nanjing Street 155, Heping District, Shenyang 110001, PR China. Electronic address:
The complement system, a cornerstone of innate immunity, plays pivotal roles in both defense and pathology, particularly through its anaphylatoxins, C3a and C5a. These small peptides, generated during complement activation, not only mediate pro-inflammatory responses but also contribute to the progression of various cancers by modulating the tumor microenvironment (TME). Anaphylatoxins influence tumor cell proliferation, epithelial-mesenchymal transition, angiogenesis, immune suppression, and therapy resistance via key signaling pathways such as PI3K/AKT, MEK/ERK, and p38 MAPK.
View Article and Find Full Text PDFBiomolecules
July 2025
Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China.
Idiopathic pulmonary fibrosis (IPF) is characterized by excessive extracellular matrix (ECM) deposition driven by aberrant fibroblast-to-myofibroblast transition (FMT). However, the upstream regulators and downstream effectors of this process remain incompletely understood. Here, we identify acyl-CoA synthetase long-chain family member 4 (ACSL4), a lipid metabolic enzyme, as a critical mediator linking complement component 5a (C5a)/C5a receptor 1 (C5aR1) signaling to FMT via calcium signaling.
View Article and Find Full Text PDFInt Immunopharmacol
August 2025
Department of Phase I Clinical Trial Center, Beijing Shijitan Hospital, Capital Medical University, Beijing 100038, China. Electronic address:
Background: The complement-activated product (C5a) is a key mediator in the pathogenesis of acute respiratory distress syndrome (ARDS). While blocking C5a represents a promising therapeutic strategy, novel anti-C5a therapies require further development.
Purpose: This study aimed to develop a novel, human anti-C5a monoclonal antibody (STSA-1002) and evaluate its efficacy in treating ARDS through in vitro and vivo studies.
Surv Ophthalmol
August 2025
Department of Ophthalmology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China; Eye School of Chengdu University of Traditional Chinese Medicine, China. Electronic address:
Retinal degenerative diseases (RDD) are a group of age-related blinding eye diseases characterized by progressive degeneration and functional impairment of retinal photoreceptors or ganglion cells, for which there are currently no effective treatments. The complement system is an important innate immune system in the human body, activated through 3 pathways (classical pathway, lectin pathway, and alternative pathway) to ultimately form a membrane attack complex that acts on target cells. Microglia are the innate immune cells of the retina, responsible for maintaining retinal homeostasis.
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