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Updated: Apr 26, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Effects of TLR4 on β2-glycoprotein I-induced bone marrow-derived dendritic cells maturation
Jingjing Liu1, Chao He2, Hong Zhou1
1Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212013, PR China; Department of Clinical Laboratory and Hematology, School of Medical Science and Laboratory Medicine of Jiangsu University, Zhenjiang, Jiangsu 212013, PR China.
Our previous study has demonstrated that Toll-like receptor 4 (TLR4) can contribute to anti-β2-glycoprotein I/β2-glycoprotein I (anti-β2GPI/β2GPI)-induced tissue factor (TF) expression in human acute monocytic leukemia cell line THP-1. However, the role of TLR4 in the activation of autoimmune response in antiphospholipid syndrome (APS) has rarely been reported. In this study, we focused on the role of TLR4 in β2GPI-induced maturation of bone marrow-derived dendritic cells (BMDCs). iDCs from C3H/HeN mice stimulated with β2GPI were more mature than that from C3H/HeJ mice, yields of CD11c(+)MHCII(+)DCs, CD11c(+)CD80(+)DCs and CD11c(+)CD86(+)DCs and production of some pro-inflammatory cytokines in iDCs from C3H/HeN were higher than those from C3H/HeJ (p<0.05). Moreover, the ability of β2GPI-treated iDCs from C3H/HeJ to stimulate proliferation of allogeneic mixed lymphocytes was lower than that of iDCs from C3H/HeN. In conclusion, our results indicate that TLR4 may play a significant role in β2-glycoprotein I-induced BMDCs maturation.
Our previous study has demonstrated that Toll-like receptor 4 (TLR4) can contribute to anti-β2-glycoprotein I/β2-glycoprotein I (anti-β2GPI/β2GPI)-induced tissue factor (TF) expression in human acute monocytic leukemia cell line THP-1. However, the role of TLR4 in the activation of autoimmune response in antiphospholipid syndrome (APS) has rarely been reported. In this study, we focused on the role of TLR4 in β2GPI-induced maturation of bone marrow-derived dendritic cells (BMDCs). iDCs from C3H/HeN mice stimulated with β2GPI were more mature than that from C3H/HeJ mice, yields of CD11c(+)MHCII(+)DCs, CD11c(+)CD80(+)DCs and CD11c(+)CD86(+)DCs and production of some pro-inflammatory cytokines in iDCs from C3H/HeN were higher than those from C3H/HeJ (p<0.05). Moreover, the ability of β2GPI-treated iDCs from C3H/HeJ to stimulate proliferation of allogeneic mixed lymphocytes was lower than that of iDCs from C3H/HeN. In conclusion, our results indicate that TLR4 may play a significant role in β2-glycoprotein I-induced BMDCs maturation.
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