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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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Immunological memory, a pivotal pillar of the adaptive immune system, is responsible for the body's ability to remember and respond more swiftly and effectively to previously encountered pathogens. This remarkable feature is what makes vaccines so effective in preventing diseases.
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Cells of the Adaptive Immune Response01:23

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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...
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Related Experiment Video

Updated: Dec 22, 2025

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
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Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice

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CD25-Targeted IL-2 Signals Promote Improved Outcomes of Influenza Infection and Boost Memory CD4 T Cell Formation.

Fahmida Alam1, Ayushi Singh1, Valeria Flores-Malavet1

  • 1Immunity and Pathogenesis Division, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL 32827.

Journal of Immunology (Baltimore, Md. : 1950)
|May 8, 2020
PubMed
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Interleukin-2 complexes (IL-2C) targeting regulatory T cells surprisingly induce inflammation but reduce lung damage in influenza A virus infection. This approach enhances T cell memory while mitigating immunopathology.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Interleukin-2 (IL-2) is a cytokine with dual pro- and anti-inflammatory roles.
  • IL-2-monoclonal antibody complexes (IL-2C) can target IL-2 to specific cell populations.
  • The JES6-1-IL-2C complex is known for inducing regulatory CD4 T cell expansion.

Purpose of the Study:

  • To investigate the inflammatory effects of an anti-inflammatory IL-2C (JES6-1-IL-2C).
  • To evaluate the impact of IL-2C on influenza A virus infection and associated immunopathology.
  • To explore the potential of IL-2C in improving T cell memory response.

Main Methods:

  • Treatment of mice with pro- and anti-inflammatory IL-2C.
  • Analysis of inflammatory protein expression.
  • Assessment of lung immunopathology in influenza A virus-infected mice.
  • Evaluation of CD4 T cell survival and memory fitness.

Main Results:

  • Anti-inflammatory JES6-1-IL-2C surprisingly induced a broad range of inflammatory factors.
  • Treatment with JES6-1-IL-2C reduced lung immunopathology in influenza A virus-infected mice.
  • IL-2C treatment enhanced CD4 T cell survival and memory fitness against influenza A virus.

Conclusions:

  • Targeting IL-2 with specific mAbs can modulate immune responses in vivo.
  • Anti-inflammatory IL-2C has a dual effect of inducing inflammation but reducing pathology in viral infections.
  • IL-2C represents a novel strategy to enhance pathogen-specific T cell memory while controlling immunopathology.