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Related Concept Videos

Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
T Cell Types and Functions01:24

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...
T Cell Activation and Clonal Selection01:22

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...
Autophagic Cell Death01:18

Autophagic Cell Death

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Generation of Human Chimeric Antigen Receptor Regulatory T Cells
10:29

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Published on: January 3, 2025

Chaperone-mediated autophagy is required for regulatory T cell function.

Ranee Harrison1, Floralba Gjergjova2, Sandra Pelka2

  • 1Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.

Nature Communications
|May 22, 2026
PubMed
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Chaperone-mediated autophagy (CMA) is vital for regulatory T cell (Treg) function and maintaining immune tolerance. CMA deficiency in Tregs leads to chronic inflammation and reduced lifespan in mice.

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Published on: October 28, 2019

Area of Science:

  • Immunology
  • Cellular Biology
  • Autophagy Research

Background:

  • Chaperone-mediated autophagy (CMA) is a lysosomal degradation pathway crucial for protein quality control and cellular processes, declining with age.
  • CMA plays a role in helper T cell activation, but its function in regulatory T cells (Tregs) remains uncharacterized.

Purpose of the Study:

  • To investigate the role of CMA in the generation and function of regulatory T cells (Tregs).
  • To determine the impact of CMA deficiency on Treg-mediated immune suppression and peripheral tolerance.

Main Methods:

  • Utilized a Treg-specific CMA-deficient mouse model.
  • Assessed Treg function in vivo using experimental models of inflammatory bowel disease and tumor-induced immune response.
  • Performed comparative quantitative proteomic analysis to identify CMA-degraded proteins and affected pathways.

Main Results:

  • CMA activity increases upon Treg activation and is essential for Treg function and peripheral tolerance.
  • CMA-deficient Tregs exhibit reduced suppressive activity in vivo.
  • Mice with CMA-defective Tregs display chronic inflammation and reduced survival with age.

Conclusions:

  • CMA is a critical regulator of Treg homeostasis and function, essential for maintaining immune tolerance.
  • Deficiency in CMA impairs Treg suppressive capacity, leading to inflammatory conditions.
  • This study reveals a novel role for CMA in Treg biology and immune regulation.