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Related Concept Videos

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...
Diversity of Antigen Receptors01:28

Diversity of Antigen Receptors

Antigen receptors are essential components of the immune system crucial in defending the body against foreign invaders. These receptors are present on the surface of B and T cells, enabling them to recognize antigens and mount an appropriate immune response.
Before encountering any antigen, lymphocytes express these receptors. On B cells, the antigen receptor is a membrane-bound antibody molecule called BCR; on T cells, it is a T cell receptor or TCR. B and T cell receptors are composed of two...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview
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...

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Related Experiment Video

Updated: Jul 19, 2026

Retroviral Transduction of T-cell Receptors in Mouse T-cells
10:14

Retroviral Transduction of T-cell Receptors in Mouse T-cells

Published on: October 22, 2010

Designer T cells by T cell receptor replacement.

Daniel Sommermeyer1, Julia Neudorfer, Monika Weinhold

  • 1Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.

European Journal of Immunology
|October 20, 2006
PubMed
Summary

T cell receptor (TCR) gene transfer can lead to mixed TCR heterodimers, impairing T cell function. Some TCRs dominate cell surface expression, altering antigen specificity and enabling designer T cell development for targeted therapies.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Biotechnology

Background:

  • T cell receptor (TCR) gene transfer is crucial for generating antigen-specific T cells in adoptive therapy.
  • Co-expression of multiple TCRs can lead to mixed TCR heterodimers, potentially compromising T cell function and specificity.

Purpose of the Study:

  • To investigate the impact of co-expressing multiple TCRs on T cell surface expression and antigen specificity.
  • To understand the preferential expression of certain TCRalpha/beta combinations in engineered T cells.

Main Methods:

  • Utilized five distinct TCRs and four different T cell types (mouse and human).
  • Analyzed cell surface expression levels of co-expressed TCRs.
  • Assessed the resulting antigen specificity of engineered T cells.

Main Results:

  • Demonstrated that certain TCRs exhibit strong cell surface expression, leading to the replacement of weaker TCRs.
  • Observed that this TCR dominance can alter the T cell's antigen specificity.
  • Showcased instances of preferential TCR expression, including a mouse TCR replacing human TCR on human T cells.
  • Found that two strong TCRs can be co-expressed effectively.

Conclusions:

  • TCR gene transfer requires careful consideration of TCR expression strength to avoid unwanted heterodimer formation and specificity exchange.
  • Preferential TCR expression mechanisms warrant further investigation.
  • Findings support the future development of engineered 'designer' T cells with tailored tumor reactivity through precise TCR selection and engineering.