Autoantibodies to CCL3 are of low sensitivity and specificity for the diagnosis of type 1 diabetes

Type 1 diabetes (T1D) is a T cell–dependent tissue-specific autoimmune disease, characterized by the selective destruction of the β cells of the pancreatic islets of Langerhans. Recently, contradictory findings have been reported about the relationship of autoantibodies to CC chemokine 3 (CCL3) and T1D, which need to be confirmed by more investigations in larger cohorts. The aim of our research was to investigate whether autoantibodies to CCL3 are useful markers for T1D in a large cohort of Chinese patients. We analyzed autoantibodies to CCL3, glutamic acid decarboxylase(GADA), insulinoma-associated protein-2 (IA-2A), and zinc transporter-8 (ZnT8A) by a radioimmunoprecipitation assay in 290 T1D subjects, 200 subjects with type 2 diabetes (T2D), 210 subjects with other diseases, and 178 healthy control subjects. Results showed that the frequencies of autoantibodies to CCL3 in subjects with T1D, T2D, and healthy control subjects were similar [3.10% (9/290), 2.50% (5/200), and 0.56% (1/178), respectively, P = 0.189]. Autoantibodies to CCL3 were not significantly different between T1D patients with or without GADA, IA-2A, or ZnT8A antibodies (2.7% vs. 3.9%, P = 0.725). In contrast, patients with systemic lupus erythematosus and rheumatoid arthritis showed higher positivity for autoantibodies to CCL3 than healthy control subjects [15.6% (5/32) and 12.5% (8/64) vs. 0.56% (1/178), all P = 0.000], and higher titer of autoantibodies to CCL3 than T1D patients (median 0.9633 and 0.4095 vs. 0.0873, P = 0.012 and P = 0.034, respectively). We conclude that autoantibodies to CCL3 are of low sensitivity and specificity for T1D and cannot be used in the diagnosis of T1D.