4. DISCUSSION
This study first analyzed the association of serum C1q levels with
disease activity in a large sample of Chinese TA patients. Our
experimental results showed that serum C1q levels were increased in TA
patients compared to healthy controls. Notably, TA patients with active
disease had higher levels of serum C1q than patients who had inactive
disease. Serum C1q levels and traditional inflammatory biomarkers in TA
patients correlated positively; therefore, our findings show that serum
C1q concentrations is a potential biomarker for evaluating disease
activity in TA patients. TA is a systemic autoimmune vasculitis with
unknown etiology. Immune mechanisms appear to be involved in TA
pathogenesis, as inflammatory cell infiltration along with granulomatous
inflammation and excessive proinflammatory cytokine productions are
observed in the vascular tissue involved.15 The
pathogenesis of systemic vasculitides, including TA, correlates with the
presence of inflammatory cells in the arteries and with immune complex
(IC) deposition, which cause activation of the complement system,
followed by the inflammation and destruction of vascular mural
structures.16 Previous studies have found ICs in TA
patient sera and on peripheral blood lymphocyte Fc
receptors.17 Additionally, a recent paper analyzed the
proteomics of circulating ICs in the sera of TA patients and identified
three unique antigens.18 Although there are some
studies on the relationship between IC and TA, analyses of the
association between the complement system and TA have not been reported
to date. Moreover, whether activation of the complement system is
involved in the pathogenesis of TA remains unclear. C1q, historically
viewed as the initiating component of the classical complement pathway,
has a diverse range of functions in both innate and acquired immunity.
Indeed, C1q plays important roles in the pathogenesis of autoimmune
diseases, particularly systemic lupus erythematosus
(SLE).19 However, the relationship between C1q and TA
remains unresolved. This study is the first to investigate the serum C1q
level in Chinese TA patients and its role in the assessment of TA
disease activity.
Several studies have suggested the use of serum C1q as an inflammatory
marker in multiple diseases. For example, the C1q level in serum is
considered an inflammatory marker for disease activity in childhood
LN7 and PM/DM.10 Our study found
that TA patients with active disease had higher levels of serum C1q than
patients who had inactive disease. At the same time, treatment-naïve
patients had higher serum C1q levels than those who had always been
treated with corticosteroids or at least one immunosuppressant. We found
serum C1q levels to correlate significantly with Kerr’s score, ESR and
hs-CRP levels in our TA patients. The AUC ofC1qwas lower than that of
ESR, but the AUC of C1q was higher than that of hs-CRP. In addition,
when the three indicators (C1q, ESR and hs-CRP) were combined, the AUC
increased, and a serum cutoff value of 167.15 mg/L C1q maximized the
disease activity assessment capacity. The sensitivity of C1q was lower
than that of ESR and higher than that of hs-CRP, though the specificity
of C1q was lower than that of both ESR and hs-CRP. Additionally, when
the three indicators (C1q, ESR and hs-CRP) were combined, the
sensitivity increased. Therefore, hs-CRP has the highest specificity,
and the sensitivity of combining three indicators (C1q, ESR and hs-CRP)
was the highest. Based on the above, we conclude that the concentration
of serum C1qisa potential inflammatory marker for TA and that the
combination of the above three indicators increases the sensitivity of
disease activity assessment.
A limitation of this study is that we did not detect C1q deposited in
vascular tissue. As a result, well-designed prospective studies should
be performed to clarify the exact clinical molecular mechanisms of C1q
in TA patients and the association with TA disease activity.