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Related Concept Videos

Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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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.
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T Cell Types and Functions01:24

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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

Updated: Jan 16, 2026

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Microbiota-induced T cell plasticity enables immune-mediated tumour control.

Tariq A Najar1, Yuan Hao2,3, Yuhan Hao4,5

  • 1Department of Cell Biology, New York University School of Medicine, New York, NY, USA.

Nature
|January 14, 2026
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Summary

Segmented filamentous bacteria (SFB) colonization enhances anti-programmed cell death protein 1 (PD-1) therapy efficacy by educating T helper 17 (TH17) cells. These gut-educated cells become T helper 1 (TH1)-like cells, boosting anti-tumour immunity and CD8+ T cell responses.

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Area of Science:

  • Immunology
  • Microbiome Research
  • Cancer Therapy

Background:

  • Immune checkpoint blockade (ICB) revolutionizes cancer care but has limited response rates.
  • The gut microbiota influences immune function and response to cancer immunotherapy.
  • Mechanisms by which gut bacteria affect ICB efficacy remain unclear.

Purpose of the Study:

  • To investigate how colonization with segmented filamentous bacteria (SFB) impacts ICB efficacy.
  • To elucidate the cellular mechanisms by which SFB influences anti-tumour immunity.

Main Methods:

  • Utilized SFB colonization in mice with implanted SFB antigen-expressing melanoma.
  • Employed T cell receptor (TCR) clonal lineage tracing, fate mapping, and MHC tetramer staining.
  • Investigated the role of SFB-induced T helper 17 (TH17) cells and their derivatives.

Main Results:

  • Anti-programmed cell death protein 1 (PD-1) therapy was effective only in SFB-colonized mice.
  • SFB induced antigen-specific T helper 1 (TH1)-like cells derived from TH17 cells in the gut.
  • These TH1-like cells promoted anti-tumour immunity by enhancing CD8+ T cell responses within the tumour microenvironment.

Conclusions:

  • A single gut commensal (SFB) can imprint T cell plasticity, potentiating PD-1 blockade efficacy.
  • SFB-induced T cell differentiation is crucial for anti-tumour immune responses and ICB effectiveness.
  • Targeted microbiota modulation represents a potential strategy to improve ICB outcomes in cancer patients.