Research Paper Volume 13, Issue 4 pp 5069—5086

Inhibiting Th1/2 cells influences hepatic capillarization by adjusting sinusoidal endothelial fenestrae through Rho-ROCK-myosin pathway

Schematic of the interaction between Th1/Th2 cells and LSECs and the mechanism underlying this interaction. (A) Interaction between Th1/Th2 cells and LSECs. (B) Pattern of cytoskeletal alteration mediated by the Rho-ROCK-myosin pathway. Interactions between Th1/2 cells and LSECs exerted different effects. Specifically, interactions between Th2 cells and LSECs activated the signal pathway to promote phosphorylation of myosin light chain (MLC), hence causing the contraction of cytoskeletal actin around LSECs and subsequent defenestration, however interactions between Th1 cells and LSECs exerted an opposite effect. MLCP, myosin light chain phosphatase.

Figure 8. Schematic of the interaction between Th1/Th2 cells and LSECs and the mechanism underlying this interaction. (A) Interaction between Th1/Th2 cells and LSECs. (B) Pattern of cytoskeletal alteration mediated by the Rho-ROCK-myosin pathway. Interactions between Th1/2 cells and LSECs exerted different effects. Specifically, interactions between Th2 cells and LSECs activated the signal pathway to promote phosphorylation of myosin light chain (MLC), hence causing the contraction of cytoskeletal actin around LSECs and subsequent defenestration, however interactions between Th1 cells and LSECs exerted an opposite effect. MLCP, myosin light chain phosphatase.