T Cells Contribute to Tumor Progression by Favoring Pro-Tumoral Properties of Intra-Tumoral Myeloid Cells in a Mouse Model for Spontaneous Melanoma
2011

T Cells Help Tumors Grow by Changing Myeloid Cell Behavior

Sample size: 29 publication 10 minutes Evidence: moderate

Author Information

Author(s): Lengagne Renée, Pommier Arnaud, Caron Jonathan, Douguet Laetitia, Garcette Marylène, Kato Masashi, Avril Marie-Françoise, Abastado Jean-Pierre, Bercovici Nadège, Lucas Bruno, Prévost-Blondel Armelle

Primary Institution: INSERM, U1016, Institut Cochin, Paris, France

Hypothesis

Do T cells influence the behavior of myeloid cells in tumors to promote cancer progression?

Conclusion

The study found that T cells can enhance the pro-tumoral properties of myeloid cells, which may contribute to tumor growth.

Supporting Evidence

  • T cells can promote the polarization of myeloid cells towards a pro-tumoral phenotype.
  • Myeloid cells from tumors inhibit T cell functions, creating a feedback loop that supports tumor growth.
  • Depletion of T cells in mice led to a decrease in tumor growth, suggesting their role in promoting cancer.
  • CD11b+ myeloid cells were found to be the most abundant population in tumor infiltrates.

Takeaway

T cells, which are usually thought to fight cancer, can actually help tumors grow by changing the behavior of certain immune cells called myeloid cells.

Methodology

The study used a mouse model of spontaneous melanoma to analyze the interactions between T cells and myeloid cells in the tumor microenvironment.

Potential Biases

Potential bias in interpreting the role of T cells due to the specific mouse model used.

Limitations

The study was conducted in a mouse model, which may not fully replicate human cancer biology.

Participant Demographics

MT/ret transgenic mice aged 3 to 6 months were used in the study.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0020235

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication