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Related Experiment Video

Updated: May 24, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Published on: June 22, 2016

LYP inhibits T-cell activation when dissociated from CSK.

Torkel Vang¹, Wallace H Liu, Laurence Delacroix

¹Infectious and Inflammatory Disease Center, Sanford-Burnham Medical Research Institute, La Jolla, California, USA.

Nature Chemical Biology

|March 20, 2012

Summary

Lymphoid tyrosine phosphatase (LYP) and C-terminal Src kinase (CSK) form a complex that regulates T-cell receptor (TCR) signaling. Dissociation of this complex allows LYP to inhibit T-cell activation, offering a potential therapeutic target for autoimmune diseases.

Related Experiment Videos

Last Updated: May 24, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Published on: June 22, 2016

Area of Science:

Immunology
Molecular Biology
Biochemistry

Background:

T-cell receptor (TCR) signaling is tightly regulated by negative feedback mechanisms.
Lymphoid tyrosine phosphatase (LYP) and C-terminal Src kinase (CSK) form a complex that inhibits TCR signaling.
Dysregulation of TCR signaling is implicated in autoimmune diseases.

Purpose of the Study:

To investigate the spatiotemporal dynamics of the LYP-CSK complex in T cells.
To understand the role of LYP-CSK complex dissociation in TCR signaling modulation.
To develop a chemical probe for LYP to explore its therapeutic potential.

Main Methods:

Studied the spatiotemporal dynamics of the LYP-CSK complex in T cells.
Developed a potent and selective chemical probe targeting LYP.
Assessed the effect of LYP inhibition on T-cell activation.

Main Results:

Dissociation of the LYP-CSK complex is essential for LYP recruitment to the plasma membrane.
Recruited LYP effectively downmodulates TCR signaling.
LYP inhibition by a chemical probe suppressed T-cell activation.
A LYP polymorphism impairing CSK binding is linked to increased autoimmune disease risk.

Conclusions:

LYP-CSK complex dissociation is a critical step in regulating T-cell activation.
Targeting LYP offers a potential therapeutic strategy for autoimmune conditions like type 1 diabetes and rheumatoid arthritis.
The developed LYP chemical probe serves as a foundation for novel autoimmunity treatments.