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            <title xml:lang="en">New insights into macrophage heterogeneity in rheumatoid arthritis</title>
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            <idno type="halRefHtml">&lt;i&gt;Joint Bone Spine&lt;/i&gt;, 2020, 88 (1), pp.105091. &lt;a target="_blank" href="https://dx.doi.org/10.1016/j.jbspin.2020.105091"&gt;&amp;#x27E8;10.1016/j.jbspin.2020.105091&amp;#x27E9;&lt;/a&gt;</idno>
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                <term xml:lang="en">Heterogeneity</term>
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                <term xml:lang="en">Rheumatoid arthritis</term>
                <term xml:lang="en">Synovium</term>
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              <p>&lt;div&gt;&lt;p&gt;Rheumatoid arthritis (RA) is a prototypic autoimmune disease that primarily affects joints. Clinical studies and animal models evidenced that mononuclear phagocytes including monocytes and macrophages are crucial to RA pathogenesis, contributing to inflammation and destruction of cartilage and bone. The last decade of research has tremendously changed our view on the origin of tissue-resident macrophages. In light of the recent publications that reveal important phenotypic and functional heterogeneity among macrophages, it is of paramount importance to identify the synovial macrophage subsets that might amplify the inflammatory response or promote the restoration of tissue homeostasis. In this review, we highlight latest studies applying single-cell RNA sequencing that provide deeper insights in macrophage subsets and their putative functions within both human and mouse synovial joint tissue.&lt;/p&gt;&lt;/div&gt;</p>
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