Abstract
Objective Transferring fibromyalgia patient IgG to mice induces pain-like behaviour and fibromyalgia IgG binds mouse and human satellite glia cells (SGCs). These findings suggest that autoantibodies could be part of fibromyalgia pathology. However, it is unknown how frequently fibromyalgia patients have anti-SGC antibodies and how anti-SGC antibodies associate with disease severity.
Methods We quantified serum or plasma anti-SGC IgG levels in two fibromyalgia cohorts from Sweden and Canada using an indirect immunofluorescence murine cell culture assay. Fibromyalgia serum IgG binding to human SGCs in human dorsal root ganglia tissue sections was assessed by immunofluorescence (n=14/group).
Results In the cell culture assay anti-SGC IgG levels were increased in both fibromyalgia cohorts compared to controls. Elevated anti-SGC IgG was associated with higher levels of self-reported pain in both cohorts, and higher fibromyalgia impact questionnaire scores and increased pressure sensitivity in the Swedish cohort. Anti-SGC IgG levels were not associated with fibromyalgia duration. Swedish FM patients were clustered into FM-severe and FM-mild groups and the FM-severe group had elevated anti-SGC IgG compared to the FM-mild and controls. Anti-SGC IgG levels detected in culture were positively correlated with increased binding to human SGCs. Moreover, the FM-severe group had elevated IgG binding to human SGCs compared to the FM-mild and control groups.
Conclusions A subset of fibromyalgia patients have elevated levels of anti-SGC antibodies, and the antibodies are associated with more severe fibromyalgia severity. Screening fibromyalgia patients for anti-SGC antibodies could provide a path to personalized treatment options that target autoantibodies and autoantibody production.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
↵* Shared last authorship
Financial support: Swedish Research Council grant 542-2013-8373 (to CIS) and grant 2016-01556 (to E Kosek), the Knut and Alice Wallenberg Foundation (018.0161 to CIS), the Karolinska Institute Foundations (to CMU), the European Union Seventh Framework Programme (FP7/2007–2013) under grant agreement number 602919 (to CIS and E Kosek), European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Grant Agreement number 764860 (to CIS and E Kosek), the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme under the grant agreement no. 866075 (to CIS), by a generous donation from Leif Lundblad and family (to CIS and E Kosek), Stockholm County Council (grant ALF-20190039 to E Kosek) grant from Fibromyalgiförbundet (E Kosek), a CIHR postdoctoral fellowship (MFE-171299 to E Krock), grants from the Karolinska Institutet Rheumatology Foundation and the Alex and Eva Wallström Foundation (E Krock), Pfizer Canada Professorship in Pain Research (to LD), Canadian Excellence Research Chairs grant CERC09 (to LD), Canadian Institutes of Health Research Strategy for Patient-Oriented Research in Chronic Pain grant SCA-145102 (to LD).
Conflicts of interest: None.