Association of circulating CXCL10 and CXCL11 with systemic sclerosis

Systemic sclerosis (SSc) is an autoimmune disorder defined ‘vascular’ disease1 due to early defective angiogenesis ending in severe multiorgan fibrosis.2 Biomarker(s) mirroring early microvascular derangements in SSc,3 potentially useful for very early diagnosis, are lacking. C-X-C angiostatic chemokines induced by interferon-γ, like CXCL10 and CXCL11, are involved in vasculopathy and associate with more severe SSc.4 5 We investigated whether the shift from very early diagnosis of SSc (VEDOSS), when vasculopathy and fibrosis are at very low degree, to definite SSc elicits serum CXCL10/CXCL11 modifications. CXCL10/CXCL11 were measured by multiplatform bead array in 26 healthy subjects; 62 sera from women admitted to the Scleroderma Clinic of Policlinico Umberto I, Sapienza University of Rome: 34 sera were from VEDOSS6 (mean age 50.50±13.66 years, mean disease duration 11.1±4.2 months) and 28 sera from patients with SSc (mean age 56.56±12.45 years, mean disease 91.3±11.73 months) fulfilling the new American College of Rheumatology/European League Against Rheumatism 2013 classification7; table 1 reports patient characteristics. Within VEDOSS, 29 subjects had a second blood sample collected during follow-up (T1, 40.67±5.46 months); for each one, we compared baseline (T0) and T1 serum chemokines. Informed consent was obtained