Complement proteins are elevated in patients with axSpA compared with relevant controls with low back pain and axSpA-features without axSpA.

Publikation: KonferencebidragPosterForskningpeer review

Axial spondyloarthritis (axSpA) is associated with a certain genetic predisposition, i.e., with the presence of human leukocyte antigen (HLA)-B27. However, the pathogenesis remains largely unexplained. Animal models of ankylosing spondylitis have shown inhibition of complement to be beneficial in terms of limiting structural damage (1). The lectin pathway of complement activation serves as a key component of the innate immune system and plays a pivotal role in both homeostasis and development. The influence of complement in axSpA is mainly unexplored. We have, however, previously reported elevated plasma levels of the lectin pathway proteins L-ficolin and H-ficolin in patients with axSpA compared with blood donors (2).

Our aim was to investigate plasma levels of lectin pathway proteins in a clinical cohort of patients with axSpA and compare them to relevant controls that we often experience significant challenges in differentiating from axSpA.

Plasma samples were obtained from individuals in a cohort of patients suffering from low back pain (LBP) including: 1) 23 patients with axSpA, 2) 55 patients without axSpA experiencing SpA-features, and 3) 64 patients with nonspecific LBP without SpA-features or MRI findings suggestive of axSpA. Diagnosis of axSpA was based on multidisciplinary team conference consensus after 3.5 years of follow-up (3). Plasma levels of 10 lectin pathway proteins (MBL, CL-L1, H-ficolin, L-ficolin, M-ficolin, MASP-1, MASP-2, MASP-3, MAp44, and MAp19) were measured by immunoassays developed in-house.

Patient characteristics are shown in Table 1. Plasma levels of lectin pathway proteins L-ficolin, M-ficolin and CL-L1 differed significantly in the patient groups (p  0.03). L-ficolin and M-ficolin were elevated in axSpA-patients compared with patients with SpA-features but not axSpA and nonspecific LBP patients (Fig. 1). CL-L1 was elevated in axSpA-patients and patients with SpA-features without axSpA compared to nonspecific LBP patients (Fig. 1). No significant differences were observed for MBL, H-ficolin, MASP-1, MASP-2, MASP-3, MAp44, and MAp19. L-ficolin levels correlated with CRP in axSpA-patients (Spearmans rho=0.58 p=0.004). M-ficolin levels correlated weakly with CRP in nonspecific LBP patients (Spearmans rho=0.36 p=0.003). No correlation with CRP was observed for CL-L1.

L-ficolin and M-ficolin are increased in patients with axSpA when compared to relevant control cohorts of patients with LBP or with SpA-features without axSpA. Our findings support a potential pathogenic role for complement in axSpA, however, further studies are needed to elucidate the diagnostic potential of the specific complement proteins.

1. Yang C, Ding P, Wang Q, Zhang L, Zhang X, Zhao J, et al. Inhibition of complement retards ankylosing spondylitis progression. Sci Rep. 2016;
2. Troldborg A, Thiel S, Mistegaard CE, Hansen A, Korsholm TL, Stengaard-Pedersen K, et al. Plasma levels of H- and L-ficolin are increased in axial spondyloarthritis: improvement of disease identification. Clin Exp Immunol. 2020;
3. Kiil RM, Mistegaard CE, Jurik AG, Christiansen AA, Hendricks O, Schiøttz-Christensen B, et al. Diagnosing axial spondyloarthritis by multidiciplinary team conference at 3.5 years’ follow-up in a cohort of patients with disease features according to the ASAS criteria. Scand J Rheumatol. 2021;
Udgivelsesårjun. 2022
StatusUdgivet - jun. 2022
BegivenhedEULAR 2022: European Congress of Rheumatology - Copenhagen, Danmark
Varighed: 1 jun. 20224 jun. 2022


KonferenceEULAR 2022

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