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Immune-mediated inflammatory diseases, such as rheumatoid arthritis (RA) are highly context dependent. Rheumatoid arthritis patients often display very different patterns of local synovial pathology– termed fibroblast-rich, myeloid-rich and lymphoid-rich synovitis. My overarching goal is to identify the decision-making processes affecting the clinical presentation of these synovial pathotypes. Combining functional genomic approaches and histological studies in mice and humans I will discuss how cells within the inflamed synovium sense and interpret cytokine cues linked with these pathotypes. With a primary focus on cytokines that signal through the latent transcription factors STAT1 and STAT3, I will provide new insights into the potential role of protein tyrosine phosphatases as biological rheostats of Jak STAT signalling within the inflamed joint.
