Karen I Cyndari, Breanna M Scorza, Zeb R Zacharias, Danielle Pessôa-Pereira, Leela Strand, Kurayi Mahachi, Juan Marcos Oviedo, Lisa Gibbs, Katherine L Butler, Graham Ausdal, Dylan Hendricks, Rika Yahashiri, Jacob M Elkins, Trevor Gulbrandsen, Andrew R Peterson, Michael C Willey, Keke C Fairfax, Christine A Petersen
{"title":"滑液中的常驻滑膜巨噬细胞:对免疫调节的影响。","authors":"Karen I Cyndari, Breanna M Scorza, Zeb R Zacharias, Danielle Pessôa-Pereira, Leela Strand, Kurayi Mahachi, Juan Marcos Oviedo, Lisa Gibbs, Katherine L Butler, Graham Ausdal, Dylan Hendricks, Rika Yahashiri, Jacob M Elkins, Trevor Gulbrandsen, Andrew R Peterson, Michael C Willey, Keke C Fairfax, Christine A Petersen","doi":"10.1016/j.clim.2024.110422","DOIUrl":null,"url":null,"abstract":"<p><p>Resident synovial macrophages (RSMs) are anti-inflammatory, self-renewing macrophages that provide physical immune sequestration of the joint space from the peripheral immune system. Increased permeability of this structure is associated with peripheral immune cells in the synovial fluid (SF). Direct measures of synovial barrier integrity are possible with tissue histology, but after barrier breakdown, if these cells perpetuate or initiate chronic inflammation in SF remains unknown. We sought to identify RSM in human SF as an indirect measure of synovial barrier integrity. To validate findings, we created a novel ex vivo explant model using human synovium. scRNA-seq revealed these SF RSMs upregulated pro-fibrotic and pro-osteoclastic pathways in inflammatory arthritis, but not septic arthritis. Increased frequencies of RSMs in SF was associated with increased sRANKL regardless of underlying pathology. These findings suggest the frequency of RSMs in SF may correlate with synovial barrier damage and in turn, potential damage to joint structures.</p>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":" ","pages":"110422"},"PeriodicalIF":4.5000,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Resident synovial macrophages in synovial fluid: Implications for immunoregulation.\",\"authors\":\"Karen I Cyndari, Breanna M Scorza, Zeb R Zacharias, Danielle Pessôa-Pereira, Leela Strand, Kurayi Mahachi, Juan Marcos Oviedo, Lisa Gibbs, Katherine L Butler, Graham Ausdal, Dylan Hendricks, Rika Yahashiri, Jacob M Elkins, Trevor Gulbrandsen, Andrew R Peterson, Michael C Willey, Keke C Fairfax, Christine A Petersen\",\"doi\":\"10.1016/j.clim.2024.110422\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Resident synovial macrophages (RSMs) are anti-inflammatory, self-renewing macrophages that provide physical immune sequestration of the joint space from the peripheral immune system. Increased permeability of this structure is associated with peripheral immune cells in the synovial fluid (SF). Direct measures of synovial barrier integrity are possible with tissue histology, but after barrier breakdown, if these cells perpetuate or initiate chronic inflammation in SF remains unknown. We sought to identify RSM in human SF as an indirect measure of synovial barrier integrity. To validate findings, we created a novel ex vivo explant model using human synovium. scRNA-seq revealed these SF RSMs upregulated pro-fibrotic and pro-osteoclastic pathways in inflammatory arthritis, but not septic arthritis. Increased frequencies of RSMs in SF was associated with increased sRANKL regardless of underlying pathology. These findings suggest the frequency of RSMs in SF may correlate with synovial barrier damage and in turn, potential damage to joint structures.</p>\",\"PeriodicalId\":10392,\"journal\":{\"name\":\"Clinical immunology\",\"volume\":\" \",\"pages\":\"110422\"},\"PeriodicalIF\":4.5000,\"publicationDate\":\"2024-12-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical immunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.clim.2024.110422\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.clim.2024.110422","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Resident synovial macrophages in synovial fluid: Implications for immunoregulation.
Resident synovial macrophages (RSMs) are anti-inflammatory, self-renewing macrophages that provide physical immune sequestration of the joint space from the peripheral immune system. Increased permeability of this structure is associated with peripheral immune cells in the synovial fluid (SF). Direct measures of synovial barrier integrity are possible with tissue histology, but after barrier breakdown, if these cells perpetuate or initiate chronic inflammation in SF remains unknown. We sought to identify RSM in human SF as an indirect measure of synovial barrier integrity. To validate findings, we created a novel ex vivo explant model using human synovium. scRNA-seq revealed these SF RSMs upregulated pro-fibrotic and pro-osteoclastic pathways in inflammatory arthritis, but not septic arthritis. Increased frequencies of RSMs in SF was associated with increased sRANKL regardless of underlying pathology. These findings suggest the frequency of RSMs in SF may correlate with synovial barrier damage and in turn, potential damage to joint structures.
期刊介绍:
Clinical Immunology publishes original research delving into the molecular and cellular foundations of immunological diseases. Additionally, the journal includes reviews covering timely subjects in basic immunology, along with case reports and letters to the editor.