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Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

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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Updated: Jun 27, 2026

Modeling the Effects of Hemodynamic Stress on Circulating Tumor Cells using a Syringe and Needle
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Published on: April 27, 2021

Intratumoral B cells under stress.

Ziv Shulman1

  • 1Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

Cancer Cell
|June 25, 2026
PubMed
Summary
This summary is machine-generated.

Stress hormone corticosterone hinders anti-tumor immunity by suppressing B cell responses. Gut bacteria-derived phage DNA activates immune cells, leading to corticosterone release and impaired cancer immunity.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Microbiome Research

Background:

  • Stress hormones like corticosterone can impact immune function.
  • Germinal center B cell responses are crucial for effective anti-tumor immunity.
  • The interplay between gut microbiota and cancer-associated fibroblasts (CAFs) in immune suppression is not fully understood.

Purpose of the Study:

  • To investigate how stress-induced corticosterone affects germinal center B cell responses and anti-tumor immunity.
  • To identify the specific triggers and mechanisms by which corticosterone is secreted in the tumor microenvironment.
  • To elucidate the role of gut microbiota in activating immune-suppressive pathways.

Main Methods:

  • Analysis of B cell responses in the presence of corticosterone.
  • Investigating Toll-like receptor 9 (TLR9) activation by microbial DNA.
  • Assessing corticosterone secretion by cancer-associated fibroblasts (CAFs).
  • Utilizing mouse models to study gut microbiota-derived signals.

Main Results:

  • Stress-induced corticosterone was found to suppress germinal center B cell responses.
  • Impaired anti-tumor immunity was observed due to corticosterone.
  • Gut microbiota-derived phage DNA was identified as a trigger for TLR9 activation.
  • CAFs were shown to secrete corticosterone upon TLR9 activation.

Conclusions:

  • Stress significantly impairs anti-tumor immunity by suppressing B cell responses via corticosterone.
  • Gut microbiota-derived phage DNA is a critical factor initiating TLR9 activation and subsequent corticosterone release from CAFs.
  • This study reveals a novel bacteria-driven mechanism of immune suppression in cancer.