Summary
Arthritis is a common clinical feature of systemic lupus erythematosus
(SLE) and is usually non-erosive as opposed to rheumatoid arthritis
(RA). While RA synovial pathology has been extensively studied, little
is known about the pathophysiology of lupus arthritis. Here, we aimed to
explore the cytokine and cellular compartments in synovial fluids of SLE
patients with arthritic manifestations.
Acellular synovial fluid and paired serum samples from SLE patients
(n=17) were analyzed with cytokine bead array for T helper associated
cytokines. From two SLE patients, synovial fluid mononuclear cells
(SFMC) were analyzed by multiparameter flow cytometry to dissect T cell,
B cell, monocyte and dendritic cell phenotypes. SLE-derived SFMC were
further stimulated in vitro to measure their capacity for
producing IFNγ and IL-17A. All patients fulfilled the ACR 1982
classification criteria for SLE. Clinical records were reviewed to
exclude the presence of comorbidities such as osteoarthritis or overlap
with RA.
IL-17A and IL-6 levels were high in SLE synovial fluid. A clear subset
of the synovial CD4+ T cells expressed CCR6+, a marker associated with
Th17 cells. IL-17-production was validated amongst CD4+CCR6+ T cells
following in vitro stimulation. Furthermore, a strong IFNγ
production was observed in both CD4+ and CD8+ cells.
Our study shows high IL-17A and IL-6 levels in synovial fluids of
patients with lupus arthritis. The Th17 pathway have been implicated in
several aspects of SLE disease pathogenesis and
our data points to Th17 involvement also for lupus arthritis.