RESUMEN
Objective To explore the influence of IL-2 pretreatment on splenic lymphocyte following mobilization with G-CSF, which may provide a new approach to attenuate acute graft-versus-host disease (GVHD). Methods Splenic cells and na(i)ve CD4+T cells from C57BL/6N mice receiving G-CSF-mobilized were pretreated with IL-2(50 U/ml) , and cocultured with the allogeneic antigens from BALB/c mice. The proliferation responses and the polarization of T cells were determined. C57BL/6N mice were randomly divided into 4 groups: G-CSF + IL-2 group, G-CSF group, IL-2 group , control group. Results Compared with the control group, IL-4 increased obviously while IFN-γ decreased significantly in the group of G-CSF + IL-2. The proliferation responses were also suppressed in vitro. Conclusion The proliferation responses of splenic cells and naive CD4 + T cells from C57BI/6N mice receiving G-CSF-mobilized to the allogeneic antigens were significantly abrogated by the pretreatment with IL-2, T cells were polarized toward the production of type-2 cytokines. The combination of G-CSF and IL-2 is potentially synergetic in the induction of T lymphocyte immune tolerance.
RESUMEN
Objective To established the method of increasihg the proportion of T regulatory cells(Tr) to T effector cells(Te), which could suppresses allogeneic ahtigen reaction, by in vivo of glucocorti-coid (dexamethasone, DXM) combined with IL-2. Methods After combined treatment to male C57BL/6N mice (donor) with DXM(5 mg. kg-1· d-1 ) and IL-2 (300 000 IU · mouse-1·d-1) for 3 d, spleen mono-nuclear cells were made and were carried out by flow cytometry analysis. Using the spleen cells of BALB/c mice as aliogeneic antigen to stimulate the spleen cells of male C57BL/6N mice for 7 d after combined treat-ment of glucoeorticoid and IL-2, the reaction of cell proliferation was detected. Results After the treatrment of DXM and IL-2, CD4+ CD25+ Foxp3+ Tr cells in the spleen of C57BL/6N mice increased abviously. The ratio of CD25+ Foxp3+ Tr to CD4+ T cells was 24.22%±7.60% in the group of DXM combined with IL-2, while the control group was 4.02% ±0. 84% ( P =0. 01 ). Compared with the control group (0. 14±0.01 ), the ratio of Tr to Te increased obviously in the group of DXM combined with IL-2 (0.43±0. 15 ) ( P = 0.01 ). The group of DXM combined with IL-2 also expressed more glucocorticoid-induced tumor necrosis factor receptor(GITR) and alloreaction was suppressed/n vitro obviously ( P < 0. 05 ). Conclusion DXM amplifies IL-2 induced the proportion of Tr to Te, and suppresses the cell proliferation stimulated by alloge-neic antigen.