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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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Updated: Jun 2, 2026

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells

Development and Functional Characterization of Murine Tolerogenic Dendritic Cells

Published on: May 18, 2018

Mtg16/Eto2 contributes to murine T-cell development.

Aubrey Hunt¹, Melissa Fischer, Michael E Engel

¹Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

Molecular and Cellular Biology

|May 4, 2011

Summary

This summary is machine-generated.

Mtg16 is crucial for T-cell development. Mice lacking Mtg16 showed impaired thymocyte development, indicating its essential role in T-cell fate specification.

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Area of Science:

Immunology
Molecular Biology
Developmental Biology

Background:

Mtg16/Eto2 functions as a transcriptional corepressor.
Disruption of Mtg16/Eto2 is implicated in acute myeloid leukemia.
The role of Mtg16 in T-cell development was previously unclear.

Purpose of the Study:

To investigate the role of Mtg16 in T-cell development.
To elucidate the molecular mechanisms by which Mtg16 regulates T-cell fate.

Main Methods:

Utilized Mtg16-deficient mice to study T-cell development.
Performed in vivo bone marrow transplantation assays.
Conducted in vitro studies using bone marrow LSK and thymic DN1 cells.
Assessed T-cell development in response to Notch signaling.
Employed complementation assays by reexpressing Mtg16.

Main Results:

Mice lacking Mtg16 exhibited significantly reduced thymocyte development.
Mtg16-deficient cells failed to contribute effectively to thymocyte development post-transplantation.
In vitro, Mtg16(-/-) LSK and DN1 cells were unable to generate CD4(+)/CD8(+) cells under Notch signaling.
Specific domains of Mtg16 were dispensable, but its transcriptional suppression and Notch binding capacities were essential.

Conclusions:

Mtg16 is a critical regulator of T-cell development.
Mtg16 integrates signaling pathways and nuclear factors for T-cell fate specification.
Mtg16's function in T-cell development relies on its ability to suppress E2A activity and bind Notch.