Elewaut Unit - Molecular Immunology and Inflammation Unit

Research field: Mechanisms of inflammation and associated tissue damage in musculoskeletal diseases

Group leader: Prof. Dr. Dirk Elewaut

Tel: +32 9 332 22 40 - Fax:+32 9 221 76 73

Research topic:

Our unit studies the mechanisms of inflammation and associated tissue damage (cartilage/bone) in musculoskeletal diseases, particularly spondyloarthritis (SpA), osteoarthritis and rheumatoid arthritis using a translational research approach.

Specifically gut inflammation is investigated as a driver of joint inflammation in SpA: about 50% of patients with SpA have subclinical, microscopical bowel inflammation. Mesenchymal cells are crucial effector cells in the gut-joint axis in SpA. Regulatory cells by contrast, particularly invariant natural killer T (iNKT) cells, have a marked anti-inflammatory effect.

We have a longstanding interest in the biology of iNKT cells under steady state conditions and in arthritic disease. In studying how regulatory feedback mechanisms fail in arthritic disease, we have uncovered an important functional interaction between Treg cells and iNKT cells.

Another common pathogenic principle for musculoskeletal disorders is mechanical strain. In a mouse model of SpA characterized by enhanced TNF mRNA stability and spontaneous development of enthesitis, unloading inhibits enthesitis development entirely. 
We are also looking for new therapeutical opportunities to modulate cartilage and bone metabolism. Over the past years, we have established several new modes to influence human chondrocyte metabolism. We also study osteoclast formation under conditions of chronic inflammation, a particularly high risk factor for inflammation induced bone loss.

Area of expertise

  • Translational research
  • Immunoregulation
  • Biomechanical strain
  • Autoimmunity
  • Musculoskelatal diseases

Technology transfer potential

  • Novel therapeutic targets
  • Assay development
  • Mouse disease models

Selected publications

  1. De Wilde K et al. A20 inhibition of STAT1 expression in myeloid cells: a novel endogenous regulatory mechanism preventing development of enthesitis.
    Annals of the Rheumatic Diseases, 76, 585-592, 2017.
  2. Favreau M* Menu E* Gaublomme D* et al. Leptin receptor antagonism of iNKT cell function: a novel strategy to combat multiple myeloma.
    Leukemia, e-pub, 2017.* These authors contributed equally
  3. Drennan M* Govindarajan S* et al. NKT sublineage specification and survival requires the ubiquitin-modifying enzyme TNFAIP3/A20.
    Journal of Experimental Medicine, 213, 1973-81, 2016. * These authors contributed equally
  4. Van De Wiele T et al. How the microbiota shapes rheumatic diseases.
    Nature Reviews Rheumatology, 12, 398-411, 2016.
  5. Van Praet J*, Donovan E* et al. Commensal microbiota influence systemic autoimmune responses.
    EMBO Journal, 34, 466-74, 2015. *These authors contributed equally.

Histology of ankle joint (click to enlarge)

MicroCT of knee joint (click to enlarge)

VIB Grand Challenges Program

This research is part of the VIB Grand Challenges Program. More information, click here.

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