Jnk1が存在しない場合の欠陥T細胞の分化

C Dong¹, D D Yang, M Wysk

¹Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.

Science (New York, N.Y.)

|December 16, 1998

まとめ

c-Jun NH2端末キナーゼ1 (JNK1) 経路は,CD4ヘルパーT細胞の応答を調節するために重要である. その欠如は,制御不能なT細胞増殖と,TH2細胞への歪んだ分化につながります.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学
分子生物学は分子生物学である.

背景:

c-Jun NH2端末キナーゼ (JNK) 信号伝達経路は,免疫反応に関与しています.
CD4ヘルパーT (TH) 細胞は,TH1およびTH2エフェクタ細胞に微分化します.

研究の目的:

T細胞受容体によるCD4+TH細胞の活性化,増殖,アポトーシス,分化におけるJNK1の役割を調査する.

主な方法:

野生型およびJnk1-/-マウス由来活性化TH細胞におけるJNK活性性の分析.
Jnk1-/- TH細胞における増殖,活性化誘発細胞死,およびサイトカイン生成の評価.

主要な成果:

Jnk1-/- TH細胞ではJNKの活性が著しく低下した.
Jnk1-/- T細胞は,過剰増殖と活性化誘発細胞死亡の減少を示した.
Jnk1-/- T細胞は,TH2細胞に優遇的に微分化され,TH2サイトカインの生産が強化された.
Jnk1-/-細胞でNFATcの核蓄積の増加が観察されました.

結論:

JNK1シグナル伝達経路は,TH細胞の増殖とアポトーシスの制御に不可欠です.
JNK1は,TH細胞のTH1/TH2系統への分化を調節する上で重要な役割を果たしています.
JNK1シグナリングは,T細胞受容体媒介の免疫反応に影響を与える.

さらに関連する動画

15:33

Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation

Published on: August 13, 2013

07:12

Mouse Naïve CD4⁺ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

関連する概念動画

03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...

02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

01:20

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...

01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

01:22

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...

01:24

T Cell Types and Functions

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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

関連する実験動画