Background/Purpose: Spondyloarthritis (SpA) covers a group of interrelated auto-inflammatory disorders where TNFa is a central mediator of disease. T cells and macrophages are abundant in the sacroiliac joint, and macrophage infiltration is associated with global disease activity. CD163 is a scavenger receptor primarily expressed by M2c macrophages. The soluble (s) form is cleaved from the cell surface by TACE/ADAM17, the metalloproteinase also responsible for the cleavage of TNFa. In RA, sCD163 is associated with disease activity and progression[i]. The mannose receptor, CD206, is a scavenger receptor responsible for collagen internalization and mainly expressed by M2a macrophages. The soluble forms of CD206 and CD163 are suggested as novel biomarkers of M2a and M2c macrophage activity. We investigated plasma levels of sCD163 and sCD206 and their association with disease activity markers in SpA patients.

Methods: Soluble CD163 and sCD206 were measured by ELISA, in plasma (PL) and synovial fluid (SF) from 23 SpA patients with peripheral joint activity, and plasma from 30 SpA patients at initiation of anti-TNFa treatment (baseline) and after 12, 20 and 52 weeks of treatment.  Clinical disease was assessed by: BASFI, BASMI, BASDAI, ASDAS, CRP and MRI scoring of the whole spine. Statistical analyses were performed by student’s t-test and Spearman’s rank correlation.

Results: Synovial fluid levels (10.2 ±4.90 mg/l) of sCD163 were significantly increased compared with PL (2.37 ±1.05 mg/l) (p<0.001). Conversely, sCD206 levels in PL (0.25 ±0.08mg/l) were higher than in SF (0.12 ±0.07 mg/l) (p<0.01). In addition, PL levels of sCD206 correlated with sCD163 (r=-0.48, p=0.02), and CRP (r=-0.50, p=0.02). A strong correlation between PL and SF sCD206 was observed (r=0.60, p=0.003), which was not the case for sCD163. In the anti-TNFa treated cohort, PL sCD163 at baseline was not increased compared with healthy controls, and was not affected by the treatment regimen. In contrast, anti-TNFa treatment affected sCD206 PL levels, which increased significantly from baseline levels (baseline: 0.16 mg/l and at 3 months: 0.20 mg/l, p<0.0001). The high levels were sustained in the entire follow-up period. Soluble CD163 at baseline and at 12 weeks correlated weakly with the BASDAI score at 12 weeks (r=-0.41, p=0.02 and r=-0.42, p=0.02), whereas no associations were observed between sCD206 and disease activity- or MRI scores.

Conclusion: In SpA, sCD163 is not increased, but show association with disease activity measured as BASDAI. Conversely, sCD206 was decreased at baseline, but increased as a response to anti-TNFa treatment. This supports that M2 macrophages are involved in SpA, but points to differences between the two subtypes engagement.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/plasma-levels-of-the-m2-macrophage-markers-cd163-and-cd206-changes-reversely-and-soluble-cd163-is-associated-with-disease-activity-in-spondyloarthritis/