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Inhibiting Th1/2 cells influences hepatic capillarization by adjusting sinusoidal endothelial fenestrae through

Yuesi Zhong1, Mingxing Xu1, Jingxiong Hu1

  • 1Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong, China.

Aging
|February 3, 2021
PubMed

Insights

T helper 1 (Th1) and Th2 cells play distinct roles in liver fibrosis by influencing hepatic capillarization. Their interactions with liver sinusoidal endothelial cells (LSECs) are mediated by the Rho-ROCK-myosin pathway, affecting liver health.

Area of Science:

  • Immunology
  • Hepatology
  • Cell Biology

Background:

  • CD4+ T cells are crucial in chronic liver diseases.
  • Hepatic capillarization is a hallmark of liver fibrosis.
  • The specific roles of Th1 and Th2 cells in this process are not well understood.

Purpose of the Study:

  • To investigate the roles of Th1 and Th2 cells in liver fibrosis.
  • To explore the interactions between Th1/Th2 cells and LSECs.
  • To determine the impact of these interactions on hepatic capillarization.

Main Methods:

  • Utilized a well-established fibrotic rat model.
  • Conducted in vitro and in vivo experiments.
  • Employed inhibitory antibodies to block Th1/Th2 cell and LSEC interactions.
  • Assessed hepatic capillarization and Rho-ROCK-myosin pathway activation.

Main Results:

  • Inhibiting Th2 cell-LSEC interaction restored fenestrae and reduced capillarization.
  • Inhibiting Th1 cell-LSEC interaction showed opposite effects.
  • Th1 cell inhibition increased Rho and myosin light chain phosphorylation; Th2 inhibition decreased it.

Conclusions:

  • Th1 and Th2 cells differentially regulate hepatic capillarization in liver fibrosis.
  • The Rho-ROCK-myosin signaling pathway likely mediates these effects.
  • Targeting Th1/Th2 cell-LSEC interactions could be a therapeutic strategy for liver fibrosis.

Keywords:
T helper cellhepatic capillarizationimmunityliver sinusoidal endothelial cellp-MLC

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