Eosinophils orchestrate cancer rejection by normalizing tumor vessels and enhancing infiltration of CD8(+) T cells.
Tumor-associated eosinophilia is frequently observed in cancer. However, despite numerous studies of patients with cancer and mouse models of cancer, it has remained uncertain if eosinophils contribute to tumor immunity or are mere bystander cells. Here we report that activated eosinophils were essential for tumor rejection in the presence of tumor-specific CD8(+) T cells. Tumor-homing eosinophils secreted chemoattractants that guided T cells into the tumor, which resulted in tumor eradication and survival. Activated eosinophils initiated substantial changes in the tumor microenvironment, including macrophage polarization and normalization of the tumor vasculature, which are known to promote tumor rejection. Thus, our study presents a new concept for eosinophils in cancer that may lead to novel therapeutic strategies.
Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Rafael
R
Carretero
Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Ibrahim M
IM
Sektioglu
Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Natalio
N
Garbi
Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Oscar C
OC
Salgado
1] Division of Translational Immunology, German Cancer Research Center, Heidelberg, Germany. [2] Regensburg Center for Interventional Immunology, University Clinic and University of Regensburg, Regensburg, Germany.
Philipp
P
Beckhove
Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany.
Günter J
GJ
Hämmerling
D000818:Animals; D001808:Blood Vessels / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002454:Cell Differentiation; D002465:Cell Movement; D002630:Chemotactic Factors / Q000276:immunology*; D003602:Cytotoxicity, Immunologic; D004804:Eosinophils / Q000276:immunology*; D008545:Melanoma / Q000098:blood supply / Q000276:immunology*; D008546:Melanoma, Experimental; D051379:Mice; D008810:Mice, Inbred C57BL; D009368:Neoplasm Transplantation; D009389:Neovascularization, Pathologic / Q000276:immunology; D018919:Neovascularization, Physiologic; D012878:Skin Neoplasms / Q000098:blood supply / Q000276:immunology*; D047368:Tumor Burden / Q000276:immunology; D059016:Tumor Microenvironment
D002630:Chemotactic Factors