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Research in the Svensson Lab

Rheumatoid arthritis (RA) is a systemic autoimmune disease that predominantly affects joints. The most prominent feature of RA is the progressive destruction of articular cartilage and bone, which is orchestrated by a subset of activated stromal cells called fibroblast-like synoviocytes (FLS). In the healthy joint, FLS control the composition of the synovial fluid and the extracellular matrix (ECM) of the joint lining. In RA, FLS become a prominent component of the joint-destructive tissue that characterizes the RA synovium and display an aggressive tumor-like phenotype including promoting inflammation, directly invading and destroying cartilage and bone. FLS are exquisitely sensitive to inflammatory cytokines and in RA the destructive action of FLS occurs in response to cytokines produced by immune cells within the rheumatoid synovium. Since FLS mediate joint destruction and amplify synovial inflammation, the development of approaches to reduce their activation and invasive potential is viewed as a high priority for the development of novel RA therapies.


Our research aims to determine the interaction between the immune system and FLS in RA, with the goal of identifying novel mechanisms of FLS activation that could serve as therapeutic targets. We have a special interest in a specific subset of innate immune cells called innate lymphoid cells (ILC). ILCs are tissue-resident immune cells that are found in most tissues of the body, where they interact with stromal cells to maintain tissue integrity. A unique feature of ILC is that they manifest a functional diversity that closely resembles what is known for T cells. Currently, ILCs are classified into five distinct subsets, ILC1, ILC2, ILC3, lymphoid tissue inducer (LTi) cells and conventional Natural Killer (cNK) cells that display immune functions like those of Th1, Th2, and Th17 subsets of CD4 T cells and CD8 killer T cells, respectively. Although ILCs have been identified in the synovial tissue of RA patients, their role in disease pathogenesis is still largely unknown.


In our research we utilize a combination of functional studies in mouse models of RA, studies on unique human patient samples and mechanistic studies in cell-based assays. By combining these studies with techniques such as multidimensional flow cytometry, multicolor fluorescent microscopy imaging as well as transcriptomic and epigenomic approaches our goal is to better understand the immunopathology of the rheumatic joint, mainly focusing on the immune-FLS interaction.

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