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A type of aplastic anemia (AA), non-severe aplastic anemia (NSAA) is defined as AA that does not meet the diagnostic criteria of severe aplastic anemia (SAA). Complement component 1q (C1q) has an important role in the pathogenesis of various autoimmune diseases; however, the role of C1q in the immune pathogenesis of NSAA is not clear. The current study aimed to determine whether C1q has an important role in the pathogenesis of NSAA. Isobaric tags for relative and absolute quantitation (iTRAQ) was used to compare the protein expression in bone marrow mononuclear cells from patients with NSAA and healthy volunteers. Pathway enrichment analysis was performed to determine the biological functions involved in NSAA. The differential expression of C1q was marked compared with other proteins. Subsequently, the concentration of C1q in serum samples was determined using ELISA and the correlation of C1q levels and NSAA severity was evaluated. The serum concentrations of C1q were significantly lower in untreated patients with newly diagnosed NSAA compared with NSAA cases in remission and normal controls. Furthermore, there was no significant difference in C1q concentration between newly diagnosed patients with NSAA and patients with autoimmune hemolytic anemia or immune thrombocytopenia. The serum concentration of C1q in newly diagnosed NSAA was significantly lower in patients with SAA (P<0.0001); whereas, there was no significant difference between the patients with SAA, patients with NSAA remission and normal controls (P>0.05). Additionally, the serum C1q concentration was significantly correlated with granulocyte counts, the level of hemoglobin, platelet counts, reticulocyte percentage and remission in patients with NSAA. The serum C1q concentration was also positively correlated with the myeloid/plasmacytoid dendritic cell ratio, and negatively correlated with the CD4(+)/CD8(+) ratio. These findings suggested that C1q may be a reliable serological marker for monitoring and evaluating disease severity in patients with NSAA. C1q may have an important role in the immune pathogenesis of NSAA.
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