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Updated: Sep 9, 2025

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

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Yuzhi Zhixue Granulesは,JAK/STAT経路を調節し,潰瘍性大腸炎のT細胞の分化に影響を与える

Yifan Zhang1, Chenxin He1, Yusheng Zhao2

  • 1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China.

Phytomedicine : international journal of phytotherapy and phytopharmacology
|September 4, 2025
PubMed
まとめ

Yuzhi Zhixue (YZZX) 粒子は,免疫細胞のバランスを取り戻し,JAK/ STAT経路を抑制することで,潰瘍性大腸炎 (UC) を効果的に治療します. この伝統的な中国医学は 腸内炎症の治療に 有望な効果を示しています

キーワード:
JAK/STAT信号経路についてT細胞の分化潰瘍性大腸炎ユジ・ジクシュエの粒

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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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