[Lipopolysaccharide promotes the proliferation of CD4(+) T cells by modulating the survive and cytokine secretion of dendritic cells].
Objective To explore the mechanism modulating the function of dendritic cells (DCs) and promoting the T cell response by lipopolysaccharide (LPS). Methods Splenic DCs were purified with anti-CD11c immunomagnetic beads. After DCs were stimulated with LPS, the expressions of co-stimulatory molecules CD80 and CD86 on the DCs were detected by flow cytometry. The protein levels of pro-inflammatory cytokines interleukin 4 (IL-4), IL-5, IL-6, IL-12p40, IL-12p70 and tumor necrosis factor alpha (TNF-α) in the culture supernatant were measured by ELISA. The apoptotic levels of DCs which were labeled with annexinV-FITC/PI were determined by flow cytometry. The phosphorylation level of nuclear factor κB P65 (NF-κB P65) was assessed by phos-flow. The mRNA levels of variable genes in microarray were determined by real-time PCR. The proliferation of CD4(+) T cells which were co-cultured with OVA323-329-treated DCs was analyzed by flow cytometry. Results The purity of DCs reached over 93% after isolation. LPS up-regulated the expressions of CD80 and CD86 and enhanced DCs-mediated proliferation of CD4(+) T cells. In addition, LPS increased the protein levels of IL-12p40, TNF-α and IL-6, and inhibited the apoptosis of DCs through the NF-κB signaling pathway. Conclusion LPS could enhance DC-mediated proliferation of CD4(+) T cells by modulating the DCs survival and cytokine secretion.
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Disease, Chinese Academy of Medical Sciences, Tianjin 300020, China.
Song
S
Chen
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Disease, Chinese Academy of Medical Sciences, Tianjin 300020, China.
Lisha
L
Lu
Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Weiqiang
W
Wang
Depeparment of Pathogen Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Ting
T
Xue
Depeparment of Pathogen Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Juan
J
Yu
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Disease, Chinese Academy of Medical Sciences, Tianjin 300020, China.
Zhina
Z
Sun
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Disease, Chinese Academy of Medical Sciences, Tianjin 300020, China.
Chunxiao
C
Zhao
Depeparment of Pathogen Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. *Corresponding author, E-mail: weishengwu604@163.com.
Fang
F
Liao
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism*; D003713:Dendritic Cells / Q000187:drug effects / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism
D016207:Cytokines; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B