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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.
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Cytotoxic T Cells-mediated Immune Response01:27

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Special Features of Adaptive Immunity01:20

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Transduction and Expansion of Primary T Cells in Nine Days with Maintenance of Central Memory Phenotype
08:49

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Published on: March 18, 2020

Reviving function in CD4+ T cells adapted to persistent systemic antigen.

Magali Noval Rivas1, Kathleen Weatherly, Marc Hazzan

  • 1Institute for Medical Immunology, Université Libre de Bruxelles, Gosselies 6041, Belgium.

Journal of Immunology (Baltimore, Md. : 1950)
|September 8, 2009
PubMed
Summary
This summary is machine-generated.

Chronic graft-versus-host disease involves T cells adapting to minor histocompatibility antigens (mHA). Negative costimulation prevents T cell overactivation, but blocking it triggers severe disease, revealing its crucial regulatory role.

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HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL
07:18

HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL

Published on: April 11, 2011

Area of Science:

  • Immunology
  • Transplantation Biology
  • T cell immunology

Background:

  • Chronic graft-versus-host disease (cGvHD) arises from persistent stimulation of T cells by minor histocompatibility antigens (mHA).
  • Understanding T cell adaptation to chronic antigen exposure is crucial for managing cGvHD and other immune-related disorders.

Purpose of the Study:

  • To investigate the mechanisms underlying T cell adaptation following chronic stimulation by recipient minor histocompatibility antigens (mHA) in a mouse model.
  • To elucidate the role of negative costimulation in regulating T cell function during chronic antigen presentation.

Main Methods:

  • Development of a mouse model mimicking chronic T cell stimulation by recipient mHA.
  • Analysis of gene expression profiles in adapted CD4+ T cells.
  • Experimental blockade of negative costimulation pathways.
  • Assessment of T cell effector functions, including organ infiltration, cytokine production, and graft rejection.

Main Results:

  • Chronically stimulated T cells developed a state of immune adaptation (unresponsiveness) preventing organ damage.
  • Adapted CD4+ T cells coexpressed genes for Th1 differentiation and negative costimulatory molecules.
  • Blocking negative costimulation reversed adaptation, leading to IFN-gamma production, severe wasting disease, and susceptibility to toxic shock.

Conclusions:

  • Negative costimulation is a key molecular mechanism enabling CD4+ T cells to adapt to persistent antigenic stimulation.
  • The effector functions of adapted T cells can be restored by overcoming inhibitory signals mediated by negative costimulation.
  • Targeting negative costimulation pathways offers potential therapeutic strategies for modulating T cell responses in cGvHD and other conditions.