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T Cell Activation and Clonal Selection01:22

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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.
Naive T cells that have not yet encountered an antigen express two primary CD...
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Samuel X Shi1, Yuwen Xiu1,2,3, Yan Li2

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CD4+ T cells worsen brain injury after intracerebral hemorrhage (ICH) by increasing swelling and neurological damage. Reducing these T cells improves outcomes in mouse models, highlighting their therapeutic potential.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Leukocyte infiltration exacerbates brain injury following intracerebral hemorrhage (ICH).
  • The specific role of T lymphocytes in ICH pathogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the involvement of CD4+ T cells in the development of brain injury after ICH.
  • To elucidate the mechanisms by which CD4+ T cells contribute to perihematomal edema (PHE) and neurological deficits.

Main Methods:

  • Analysis of CD4+ T cell accumulation in human ICH patients and ICH mouse models.
  • Depletion of CD4+ T cells in ICH mouse models.
  • Single-cell transcriptomic analysis of brain-infiltrating T cells.
  • Assessment of perihematomal edema (PHE) volumes and neurological deficits.

Main Results:

  • CD4+ T cells accumulate in perihematomal regions and activate concurrently with PHE development.
  • Depletion of CD4+ T cells significantly reduced PHE volumes and improved neurological function in ICH mice.
  • Single-cell transcriptomics revealed proinflammatory and proapoptotic profiles in brain-infiltrating T cells.
  • CD4+ T cells promote PHE via IL-17 release and induce endothelial cell death through TRAIL/DR5 signaling, disrupting blood-brain barrier integrity.

Conclusions:

  • CD4+ T cells play a critical role in exacerbating brain injury and edema following ICH.
  • Targeting CD4+ T cells and their effector molecules (IL-17, TRAIL) represents a promising immunomodulatory therapeutic strategy for ICH.