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T Cell Activation and Clonal Selection

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...

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Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells

Generation of Induced Regulatory T Cells from Primary Human Naïve and Memory T Cells

Published on: April 16, 2012

Aging T_regs need DCAFinating.

Dachuan Dong¹, Jonathan S Maltzman²

¹Veterans Administration Palo Alto Health Care System and Department of Medicine, Stanford University, Palo Alto, CA 94304.

Science Immunology

|October 3, 2020

Summary

This summary is machine-generated.

Loss of DCAF1 causes regulatory T cell (Treg) aging and inflammation due to reactive oxygen species (ROS). This discovery highlights a new mechanism linking DCAF1 to age-related immune dysfunction.

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Area of Science:

Immunology
Cellular Biology
Aging Research

Background:

Regulatory T cells (Tregs) are crucial for immune homeostasis.
Aging is associated with immune system decline and increased inflammation.
DCAF1 (DDB1- and CUL4-associated factor 1) is implicated in cellular processes.

Purpose of the Study:

To investigate the role of DCAF1 in Treg function and aging.
To explore the link between DCAF1, reactive oxygen species (ROS), and Treg aging.
To understand the contribution of DCAF1 loss to age-related inflammation.

Main Methods:

Utilized knockout models to study DCAF1 deficiency in Tregs.
Assessed Treg aging markers and function.
Measured levels of reactive oxygen species (ROS) in DCAF1-deficient Tregs.
Analyzed inflammatory responses in vivo and in vitro.

Main Results:

Loss of DCAF1 accelerated Treg aging.
DCAF1 deficiency led to increased ROS production within Tregs.
Elevated ROS in DCAF1-null Tregs correlated with impaired suppressive function.
DCAF1-deficient Tregs promoted a pro-inflammatory environment.

Conclusions:

DCAF1 is essential for maintaining Treg health and function during aging.
ROS accumulation resulting from DCAF1 loss drives Treg aging and inflammation.
Targeting DCAF1 or ROS may offer therapeutic strategies for age-related immune dysfunction.