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Biology subjects

Gurra, M. G.

Publications and source records attributed to Gurra, M. G..

2 recordsLinked to original sources

Comprehensive analysis of myeloid reporter mice

Macrophages are a pivotal cell type within the synovial lining and sub-lining of the joint, playing a crucial role in maintaining homeostasis of synovium. Although fate-mapping techniques have been employed to differentiate synovial macrophages from other synovial myeloid cells, no comprehensive study has yet been conducted within the mouse synovial macrophage compartment. In this study, we present, for the first time, lineage tracing results from 18 myeloid-specific fate-mapping models in mouse peripheral blood (PB) and synovial tissue. The identification of synovial macrophages and monocyte-lineage cells through flow cytometry was further validated using cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) datasets. These findings provide a valuable methodological tool for researchers to select appropriate models for studying the function of synovial myeloid cells and serve as a reference for investigations in other tissue types.

immunology↗

Tissue-resident, extravascular CD64-Ly6C- population forms a critical barrier for inflammation in the synovium

Monocytes are one of the most abundant immune cells infiltrating the inflamed organs. However, the majority of studies on monocytes focus on circulating cells, rather than those in the tissue. Here, we identify and characterize an intravascular (i.v.) and extravascular (e.v.) synovial population (Syn Ly6C- cells) which lack cell surface markers of classical monocytes (Ly6C and CD62) or tissue macrophages (CD64 and Tim4), are transcriptionally distinct and conserved in RA patients. e.v. Syn Ly6C- cells are independent of NR4A1 and CCR2, long-lived and embryonically derived while the i.v. Syn Ly6C- cells are dependent on NR4A1, short lived and derived from circulating NCM. e.v. Syn Ly6C- cells undergo increased proliferation and reverse diapedesis dependent on LFA1 in response to arthrogenic stimuli and are required for the development of RA-like disease. These findings uncover a new facet of mononuclear cell biology and are imperative to understanding tissue-resident myeloid cell function in RA.

immunology↗