4.8 Editorial Material

Comment on Tumor-initiating cells establish an IL-33-TGF-β niche signaling loop to promote cancer progression

Journal

SCIENCE
Volume 372, Issue 6538, Pages -

Publisher

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.abf2022

Keywords

-

Funding

  1. Institut National de la Sante et de la Recherche Medicale (INSERM) ATIP-Avenir program
  2. INSERM-Region Occitanie
  3. European Research Council (ERC)-Seventh Framework Program [ERC-2013-CoG 616050]
  4. Institut Pasteur
  5. INSERM
  6. Societe Francaise de Dermatologie (SFD)
  7. Societe Francaise d'Allergologie (SFA)
  8. Marie Sklodowska-Curie Individual Fellowship [749629]
  9. European Research Council [802041]
  10. INSERM ATIP-Avenir program
  11. Chancellor's Fellowship of the University of Edinburgh
  12. Kennedy Trust for Rheumatology Research
  13. Marie Curie Actions (MSCA) [749629] Funding Source: Marie Curie Actions (MSCA)
  14. European Research Council (ERC) [802041] Funding Source: European Research Council (ERC)

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The researchers found that interleukin-33 can induce accumulation of tumor-associated macrophages expressing the Fc epsilon RI receptor, but raised concerns about the specificity of the anti-Fc epsilon RI antibody used in the study.
Taniguchi et al. (Research Articles, 17 July 2020, p. 269) claim that the cytokine interleukin-33 induces accumulation of tumor-associated macrophages expressing the immunoglobulin E receptor Fc epsilon RI. Although these findings hold great therapeutic promise, we provide evidence that the anti-Fc epsilon RI antibody used in this study is not specific for Fc epsilon RI on macrophages, which raises concerns about the validity of some of the conclusions.

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