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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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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.
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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.
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Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
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Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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Cell sorting plays an...
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Related Experiment Video

Updated: May 3, 2026

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CD28 and CD3 have complementary roles in T-cell traction forces.

Keenan T Bashour1, Alexander Gondarenko, Haoqian Chen

  • 1Departments of Biomedical Engineering and Mechanical Engineering, Columbia University, New York, NY 10027.

Proceedings of the National Academy of Sciences of the United States of America
|January 29, 2014
PubMed
Summary

T cells use the T-cell receptor (TCR) and CD3 complex to sense substrate rigidity and generate forces. CD28 engagement enhances these forces via PI3K signaling, revealing insights into immune response mechanics.

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Area of Science:

  • Immunology
  • Cellular Mechanics
  • Biophysics

Background:

  • Mechanical forces regulate T-cell activation and adaptive immune responses.
  • T cells sense substrate rigidity via T-cell receptor (TCR) coreceptor CD3 and CD28.

Purpose of the Study:

  • Investigate complementary roles of CD3 and CD28 in regulating T-cell force generation.
  • Elucidate the mechanisms of T-cell force application during immune interactions.

Main Methods:

  • Traction force microscopy on primary human T cells.
  • Utilized micrometer-scale elastomer pillar arrays with activation antibodies for CD3 and CD28.
  • Manipulated antibody presentation (on pillars vs. in solution) to differentiate receptor functions.

Main Results:

  • T cells generated ~100 pN traction forces on pillars with both CD3 and CD28 antibodies.
  • Force generation is primarily linked to CD3 and the TCR complex.
  • CD28 engagement amplifies CD3-mediated forces via PI3K signaling, not increased cell-surface coupling.
  • Force generation is peripheral, involving phosphorylated Pyk2, similar to integrin signaling.
  • T cells apply forces via TCR on peptide-MHC, analogous to CD3-mediated forces.

Conclusions:

  • CD3 and CD28 have distinct, complementary roles in T-cell mechanosensing and force generation.
  • PI3K signaling mediates CD28's enhancement of TCR-driven forces.
  • T cells employ integrin-like mechanisms for force application during immune surveillance and activation.