T Zhang1, B Sun, Q Feng, Y Yuan, H Zhu, L Liu. 1. Department of Hematology, Xijing Hospital, The Fourth Military Medical University, Xian 710032, China.
Abstract
OBJECTIVE: To detect the induced levels of IL-4, IFN-gamma and TNF-alpha in the supernatant of bone marrow mononuclear cells (BMMNC) and compare the difference of immune status between acute (SAA) and chronic (CAA) aplastic anemia patients. METHODS: Concentrations of IL-4, IFN-gamma and TNF-alpha in PHA-P-induced BMMNC supernatants were determined by ELISA assay in 11 SAA and 13 CAA patients as well as 16 controls. Concentration differences between the two groups were compared. RESULTS: (1) The IFN-gamma and TNF-alpha levels in AA patients studied were much higher than that in controls, and IL-4 levels were normal in SAA group but elevated in CAA group. (2) TNF-alpha levels were comparable between the two AA groups, but both IL-4 and IFN-gamma levels were significantly different between them. CONCLUSION: Enhanced cellular immunity seems to play an important role in the pathogenesis of SAA, and enhancement of both cellular and humoral immunity might contribute to the pathogenesis of CAA.
OBJECTIVE: To detect the induced levels of IL-4, IFN-gamma and TNF-alpha in the supernatant of bone marrow mononuclear cells (BMMNC) and compare the difference of immune status between acute (SAA) and chronic (CAA) aplastic anemiapatients. METHODS: Concentrations of IL-4, IFN-gamma and TNF-alpha in PHA-P-induced BMMNC supernatants were determined by ELISA assay in 11 SAA and 13 CAA patients as well as 16 controls. Concentration differences between the two groups were compared. RESULTS: (1) The IFN-gamma and TNF-alpha levels in AA patients studied were much higher than that in controls, and IL-4 levels were normal in SAA group but elevated in CAA group. (2) TNF-alpha levels were comparable between the two AA groups, but both IL-4 and IFN-gamma levels were significantly different between them. CONCLUSION: Enhanced cellular immunity seems to play an important role in the pathogenesis of SAA, and enhancement of both cellular and humoral immunity might contribute to the pathogenesis of CAA.