Artikel
Predictive value of innate lymphoid cells in systemic sclerosis
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Autoren
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Alina Soare
- Medizinische Klinik 3, Universitätsklinikum Erlangen, Rheumatologie, Erlangen
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Stefanie Weber
- Medizinische Klinik 3, Universitätsklinikum Erlangen, Erlangen
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Simon Rauber
- Medizinische Klinik 3, Universitätsklinikum Erlangen, Erlangen
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Lisa Hambeck
- Medizinische Klinik 3, Universitätsklinikum Erlangen, Erlangen
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Georg Schett
- Universitätsklinikum Erlangen, Medizinische Klinik 3, Rheumatologie und Immunologie, Erlangen
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Jörg H. W. Distler
- Universitätsklinikum Erlangen, Medizinische Klinik 3, Rheumatologie und Immunologie, Erlangen
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Andreas Ramming
- Medizinische Klinik 3, Universitätsklinikum Erlangen, Rheumatologie, Erlangen
| Veröffentlicht: | 8. Oktober 2019 |
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Gliederung
Text
Background: Systemic sclerosis (SSc) is a chronic autoimmune disease with a high morbidity and mortality. Numerous studies have suggested that type 2 and type 3 cytokines are key drivers of progressive fibrosis. Recently, innate lymphoid cells (ILC) are emerging as an important cellular source of type 2 and type 3 cytokines triggering fibrotic tissue remodeling.
We aim in our study to evaluate the predictive role of ILC2 and ILC3 in SSc patients.
Methods: We conducted an observational retrospective study on 52 patients with SSc fulfilling the 2013 ACR/EULAR classification criteria. Blood samples collected between 15.09.2014 and 15.01.2015 were analyzed by flow cytometry and ILC2 and ILC3 counts were measured. The predictive value of ILC2 and ILC3 during a 2-year follow-up was analyzed using SPSS 21.0. ILC3 counts were analyzed in skin sections by immunofluorescence staining.
Results: 52 patients were included in the study, 78% female, 63% limited cutaneous SSc with a mean follow-up time of 2.85 ± 1.28 years. At baseline we have shown that circulating ILC2s are significantly increased compared to gender and age-matched healthy controls. Increased numbers of ILC2s significantly correlated with worsening of mRSS (p < 0.001; 95% CI 1.39 – 3.26). ILC2 counts also correlated with 5% decrease of diffusion capacity of carbon monoxide (DLCO) during the follow-up time (p < 0.0001; 95% CI 1.83 – 3.49). Worsening of forced vital capacity (FVC) over 2 years was also significantly correlated with an increased number of ILC2s (p < 0.0001; 95% CI 1.27 – 3.04). Although new appearance of digital ulcers could not be predicted by ILC2 counts, increased numbers of ILC2s were correlated with digital ulcers at follow-up. In contrast to ILC2, circulating ILC3s were not found to be correlated with worsening of disease activity. However, ILC3s were prominent in fibrotic skin of SSc patients compared to healthy controls, and showed strong production of IL-17.
Conclusion: Here, we provide first evidence for a role of ILC2s as potential prognostic marker of disease progression in SSc. ILC3s showed strong cytokine production in the fibrotic skin of SSc patients. The functional impact has to be further evaluated.
