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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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Checkpoint blockade and the stem-like T cell trade-off.

Julie M Mazet1,2,3, Johanna A Joyce1,2,3

  • 1Department of Fundamental Oncology, University of Lausanne, Switzerland.

Molecular Oncology
|April 20, 2026
PubMed
Summary
This summary is machine-generated.

Stem-like T cells are crucial for effective programmed cell death protein 1 (PD1) blockade therapy. Conventional type 1 dendritic cells (cDC1s) and PD1 signaling maintain these vital anti-tumor cells within the tumor microenvironment.

Keywords:
Stem‐like T cellscancer immunityimmune checkpoint blockade

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Area of Science:

  • Immunology
  • Cancer Biology
  • Cellular Immunology

Background:

  • Stem-like T cells are essential for sustained anti-tumor immunity during PD1 blockade.
  • The mechanisms regulating stem-like T cell maintenance in cancer are not fully understood.

Purpose of the Study:

  • To investigate the niche and regulatory mechanisms of stem-like T cells in murine cancer models.
  • To define the role of conventional type 1 dendritic cells (cDC1s) and PD1 signaling in stem-like T cell maintenance.

Main Methods:

  • High-dimensional 3D-imaging
  • Immunological profiling
  • Murine cancer models

Main Results:

  • cDC1s preserve high-affinity tumor-specific stem-like T cells by providing sustained TCR stimulation and PD-L1/2 co-inhibitory signals.
  • PD1 signaling disruption enhances effector T cell expansion but leads to stem-like T cell differentiation and apoptosis.
  • Disruption of PD1 signaling ultimately depletes the stem-like T cell pool.

Conclusions:

  • cDC1s and PD1 signaling are critical for maintaining the stem-like T cell reservoir necessary for long-term anti-tumor responses.
  • Disruption of PD1 signaling may represent a long-term vulnerability in immune checkpoint blockade therapy if tumors are not fully eradicated.