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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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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Related Experiment Video

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Generation of Human Chimeric Antigen Receptor Regulatory T Cells
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CD28 and ITK signals regulate autoreactive T cell trafficking.

Nitya Jain1, Bing Miu, Jian-kang Jiang

  • 1Department of Pathology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

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|November 26, 2013
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Blocking the ITK pathway prevents self-reactive T cells from entering tissues, halting autoimmune destruction. ITK inhibitors show promise for treating autoimmune diseases like type 1 diabetes.

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Area of Science:

  • Immunology
  • Autoimmunity
  • T cell trafficking

Background:

  • Autoimmune diseases involve self-reactive T cells attacking tissues.
  • Cytotoxic T lymphocyte antigen-4 (CTLA-4) deficiency causes fatal autoimmunity.
  • The CD28 co-stimulatory pathway influences T cell responses.

Purpose of the Study:

  • To investigate the role of the CD28-activated Tec family kinase ITK in T cell trafficking and autoimmunity.
  • To explore ITK as a therapeutic target for autoimmune disorders.

Main Methods:

  • Studied mice lacking CTLA-4 (Ctla4(-/-)) and ITK (Itk(-/-)).
  • Analyzed T cell activation, proliferation, and tissue infiltration in genetically modified mice.
  • Evaluated the efficacy of ITK inhibitors in mouse models of type 1 diabetes.

Main Results:

  • Concurrent ablation of ITK and CTLA-4 (Itk(-/-); Ctla4(-/-)) prevented T cell infiltration into nonlymphoid tissues.
  • Self-reactive T cells accumulated in lymphoid organs but did not cause disease in Itk(-/-); Ctla4(-/-) mice.
  • ITK inhibitors mimicked the protective phenotype and reduced T cell infiltration in type 1 diabetes models.

Conclusions:

  • ITK plays a critical role in licensing autoreactive T cells to traffic into tissues.
  • Inhibiting ITK offers a potential therapeutic strategy for human autoimmune diseases.
  • Targeting ITK may prevent organ-specific autoimmune destruction without compromising general immunity.