Pivotal Advance: Eosinophil infiltration of solid tumors is an early and persistent inflammatory host response

Journal of Leukocyte Biology

Katie O’Neill⁴  Stephanie Constant³  Theresa R. Lombari²  Stephania A. Cormier¹  Michael P. McGarry⁵  Sergei I. Ochkur⁵  Cheryl Protheroe⁴  Carrie Bedient⁵  Nancy A. Lee⁴  Dawn Dimina⁵  Dana Colbert⁴  Ralph Pero⁴  Thanh Nguyen⁴  Anna G. Taranova⁵  James J. Lee⁵ 

[1] Divisions of Hematology and Oncology and Department of Biological Sciences, Louisiana State University, Baton Rouge; and Divisions of Hematology and Oncology and Divisions of Hematology and Oncology and Department of Biological Sciences, Louisiana State University, Baton Rouge; and Department of Biological Sciences, Louisiana State University, Baton Rouge; and Divisions of Hematology and Oncology and Department of Biological Sciences, Louisiana State University, Baton Rouge; andLaboratory Animal Research Core (LARC) Facility, Mayo Clinic Arizona, Scottsdale; Laboratory Animal Research Core (LARC) Facility, Mayo Clinic Arizona, Scottsdale; Laboratory Animal Research Core (LARC) Facility, Mayo Clinic Arizona, Scottsdale;;Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC;Divisions of Hematology and Oncology and Divisions of Hematology and Oncology and Divisions of Hematology and Oncology and;Pulmonary Medicine and Pulmonary Medicine and Pulmonary Medicine and

关键词: tumor immunology;    cancer;    mice;    B16 melanoma cells;   

DOI  :  10.1189/jlb.0106027

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Tumor-associated eosinophilia has been observed in numerous human cancers and several tumor models in animals; however, the details surrounding this eosinophilia remain largely undefined and anecdotal. We used a B16-F10 melanoma cell injection model to demonstrate that eosinophil infiltration of tumors occurred from the earliest palpable stages with significant accumulations only in the necrotic and capsule regions. Furthermore, the presence of diffuse extracellular matrix staining for eosinophil major basic protein was restricted to the necrotic areas of tumors, indicating that eosinophil degranulation was limited to this region. Antibody-mediated depletion of CD4+ T cells and adoptive transfer of eosinophils suggested, respectively, that the accumulation of eosinophils is not associated with T helper cell type 2-dependent immune responses and that recruitment is a dynamic, ongoing process, occurring throughout tumor growth. Ex vivo migration studies have identified what appears to be a novel chemotactic factor(s) released by stressed/dying melanoma cells, suggesting that the accumulation of eosinophils in tumors occurs, in part, through a unique mechanism dependent on a signal(s) released from areas of necrosis. Collectively, these studies demonstrate that the infiltration of tumors by eosinophils is an early and persistent response that is spatial-restricted. It is more important that these data also show that the mechanism(s) that elicit this host response occur, independent of immune surveillance, suggesting that eosinophils are part of an early inflammatory reaction at the site of tumorigenesis.

【 授权许可】

Unknown