ABSTRACT
Objective:To explore the effects of suppress or enhancer of lin-12-like(Sel1L) on differentiation and function of bone marrow-derived dendritic cells.Methods:To generate conditional knockout mice by the Cre-Loxp recombination system.ELISA and Real-time fluorescence quantitative PCR(RT-PCR) was used for analyzing the protein levels and mRNA levels of IL-6/IL-12 in BMDCs.The protein levels of Sel1L in BMDCs were detected by Western bolt.The expression of CFSE,CD80,CD86,MHC-Ⅰ,MHC-Ⅱon BMDCs and the capability in priming OVA specific CD4+T cells proliferation were analyzed by the flow cytometry.Results:The deficiency of Sel1L decreases the proliferation of DCs during its differentiation,up-regulates the secretion of IL-6,IL-12 and the expression of MHC-Ⅰ.Notably,Sel1L-null DCs was failed to up-regulate MHC-Ⅱexpression and dramatically impaired their ability to prime OVA323-339specific CD4+T cell.Conclusion:The deletion of Sel1L can reduce the proliferation of BMDCs and down-regulate its ability in priming the proliferation of OVA specific CD4+T cells.
ABSTRACT
Purpose To investigate the expression and the clinical significances of SEL1L and BCL-2 in 123 cases of diffuse large B cell lymphoma (DLBCL) and cell line SUDHL-4, LY-10. Methods Immunohistochemistry staining for SEL1L was performed in 123 DLBCL and 60 reactive lymphoid hyperplasia (RLH), and also BCL-2 protein in 123 DLBCL. Immunocytochemistry staining and Western blot analysis for SEL1L protein were used in SUDHL-4 and LY-10. Results The high expression rate of SEL1L was 69.9％ in 123 DLBCL, which was significantly higher than that in 60 RLH (25.0％ ). The expression of SEL1L protein in DLBCL was not related to clinic pathological parameters. The positive rate of BCL-2 was 83.7％ in123 DLBCL. The expression of BCL-2 protein was correlated with immunophenotyping, primary location, and Ann Arbor stage. The expression of SEL1L protein was positively correlated with that of BCL-2 protein in DLBCL (r=0.227, P＜0.05). SEL1L protein was also detected in SUDHL-4 and LY-10 cell lines. Conclusion The SEL1L protein may play an important role in the carcinogenesis of DLBCL, and may be associated with BCL-2.