Systemic Lupus Erythematosus and Systemic sclerosis

Group

We focus on systemic auto-immune diseases pathophysiology of Systemic Lupus Erythematosus (SLE) and Systemic sclerosis (SSc). These diseases are characterised by the presences of auto-antibodies and can involve all different organs, which result in damage, and thus morbidity and even mortality for the patients.

With our research we aim to elucidate the pathogenesis in an early phase, for example changes in the Interferon pathway or in neutrophil extracellular trap (NET) formation, to possibly intervene in an earlier phase.

In systemic sclerosis we investigate factors that may contribute to fibrosis, especially in the lungs, leading to severe lung complications in patients with SSc.

Our main fields of research interest concern

Elucidate pathophysiology in incomplete SLE, including different pathways, such as interferon, NETS and changes in the adaptive immune system, including the B cells and their production of auto-antibodies
Finding biomarkers to predict progression to SLE
Analysing LifeLines database to discover risk factors of development of SLE
Analysing adverse pregnancy outcomes in SLE patients to elucidate the pathogenesis of pregnancy morbidity
Redox signalling and inflammation in lupus nephritis
Investigation of factors leading to fibrosis in lung tissue in SSc patients
Predictive biomarkers for complications in SSc patients

Discover our research

publication

Immunohistochemical analysis reveals higher Myxovirus resistance protein 1 expression and increased macrophage count in placentas from patients with systemic rheumatic diseases

2025, Rheumatology International

publication

Low density granulocytes and neutrophil extracellular trap formation are increased in incomplete systemic lupus erythematosus

2024, Rheumatology (Oxford, England)

All publications

Relevance

Making a difference on pathophysiology, systemic auto-immune diseases

Prevention and early recognition of diseases has high priority. Focusing on systemic lupus erythematosus (SLE), some patients with clinical symptoms and autoantibodies suggestive of SLE, do not fullfil the classification criteria for SLE. This state of disease is referred to as incomplete SLE (iSLE), and comprises a very heterogeneous group of patients of which 20 – 57% will eventually develop SLE. At this moment, it is unclear which factors determine this progression.

Ideally, a biomarker or a combination of biomarkers will indicate which patients may progress from iSLE to SLE and thereby help to understand and intervene in the pathogenesis of SLE.

We use the LifeLines cohort to analyse the presence of auto-antibodies, symptoms of SLE and other known risk factors. Thereby, we might be able to predict the development of SLE in a general population.

More information about LifeLines