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IL-17A-producing CD30(+) Vδ1 T cells drive inflammation-induced cancer progression
Yoshitaka Kimura1, Nao Nagai1, Naoki Tsunekawa1
1Laboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Cancer Science
|July 8, 2016
Summary
Inflammation promotes cancer metastasis. Interleukin-17A (IL-17A) produced by specific T cells (Vδ1T cells) drives this process, highlighting a target for cancer therapy.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Inflammation's role in tumor metastasis is suspected but not fully understood.
- The specific immune responses initiating cancer progression require elucidation.
Purpose of the Study:
- To identify the immune response critical for inflammation-induced cancer metastasis.
- To investigate the role of Interleukin-17A (IL-17A) in cancer progression.
Main Methods:
- Utilized an in vivo tumor progression model.
- Analyzed immune cell populations, cytokine production (IL-17A, IL-1β), and neutrophil infiltration.
- Investigated the role of Vδ1 T cells, TCR, MyD88/IL-23 pathway, and CD30.
Main Results:
- IL-17A is crucial for escalating cancer cell malignancy in an inflammatory microenvironment.
- Exposure duration to inflammation correlates with increased tumorigenicity.
- Vδ1 T cells produce IL-17A in a MyD88/IL-23-dependent manner, promoting inflammation.
- CD30 is identified as a key molecule in Vδ1 T cell function; its blockade inhibits cancer immune-escalation.
Conclusions:
- IL-17A-producing CD30(+) Vδ1 T cells are vital in initiating inflammation and creating a pro-cancerous microenvironment.
- Targeting the CD30 pathway on Vδ1 T cells can disrupt cancer immune-escalation.
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