Systemic sclerosis & Raynaud's
Dendritic cells drive profibrotic inflammation and aberrant T cell polarization in systemic sclerosis
Authors' conclusion
Our findings suggest that functional alterations of DCs promote immune mechanisms favouring the aberrant T cell polarization and profibrotic inflammation behind clinical SSc heterogeneity.
Study context
- Population
- Patients with limited cutaneous SSc (lcSSc), diffuse cutaneous SSc (dcSSc) and healthy controls (HCs); monocyte-derived dendritic cells (DCs) stimulated with toll-like receptor (TLR) agonists
- Comparison
- Mo-DCs from patients with lcSSc and dcSSc vs HCs
- Outcome
- Cytokine responses of stimulated Mo-DCs and their influence on T-cell cytokine production
Methodological detailsin vitro TLR stimulation, autologous Mo-DC–T cell co-culture
- In vitro TLR stimulation
- Autologous Mo-DC–T cell co-culture
Main finding
As reported in the abstract
- Increased production of Th17-related cytokines (IL-1β, IL-17F, IL-21, IL-22) by SSc vs HC Mo-DCs, varying between lcSSc vs dcSSc and early- vs late-stage subgroups
- Significant increment in IL-33 production by Mo-DCs in all SSc cases regardless of clinical phenotype
- T cells displayed Th2, Th17 and dual Th2-Th17 phenotypes after exposure to autologous TLR-stimulated Mo-DCs from SSc patients but not HCs; pronounced in early-stage dcSSc, less significant in late-stage lcSSc
Original publication
Dendritic cells drive profibrotic inflammation and aberrant T cell polarization in systemic sclerosis. Rheumatology (Oxford). Published 5 September 2022. doi:10.
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