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Eosinophils in the Tumor Microenvironment

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Tumor Microenvironment

Abstract

Eosinophils are rare blood-circulating and tissue-infiltrating immune cells studied for decades in the context of allergic diseases and parasitic infections. Eosinophils can secrete a wide array of soluble mediators and effector molecules, with potential immunoregulatory activities in the tumor microenvironment (TME). These findings imply that these cells may play a role in cancer immunity. Despite these cells were known to infiltrate tumors since many years ago, their role in TME is gaining attention only recently. In this chapter, we will review the main biological functions of eosinophils that can be relevant within the TME. We will discuss how these cells may undergo phenotypic changes acquiring pro- or antitumoricidal properties according to the surrounding stimuli. Moreover, we will analyze canonical (i.e., degranulation) and unconventional mechanisms (i.e., DNA traps, exosome secretion) employed by eosinophils in inflammatory contexts, which can be relevant for tumor immune responses. Finally, we will review the available preclinical models that could be employed for the study of the role in vivo of eosinophils in cancer.

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Abbreviations

AEC:

Absolute eosinophils count

ANGPTs:

Angiopoietins

ADCC:

Antibody-dependent cell-mediated cytotoxicity

Ag:

Antigen

APCs:

Antigen-presenting cells

A. fumigatus :

Aspergillus fumigatus

BECs:

Blood endothelial cells

BAL:

Bronchoalveolar lavage

CAFs:

Cancer-associated fibroblasts

CEL:

Chronic eosinophilic leukemia

DCs:

Dendritic cells

ECP:

Eosinophil cationic protein

EDN:

Eosinophil-derived neurotoxin

EPX:

Eosinophil peroxidase

E. coli :

Escherichia coli

EXO:

Exosomes

EV:

Extracellular vesicles

FGF:

Fibroblast growth factor

FPR-1:

Formyl peptide receptor-1

HSC:

Hematopoietic stem cell

HMGB1:

High Mobility Group Box 1

HD:

Hodgkin’s disease

HES:

Hypereosinophilic syndrome

ICIs:

Immune checkpoint inhibitors

ILC2:

Innate lymphoid cells

IFN:

Interferon

IL:

Interleukin

iNKT:

Invariant natural killer T

LIAR:

Local immunity and/or remod eling/repair

LECs:

Lymphatic endothelial cells

MBP:

Major basic protein

MCA:

Methylcholanthrene

mAb:

Monoclonal antibody

M-MDSC:

Monocytic myeloid-derived suppressor cells

MVB:

Multivesicular bodies

MDSC:

Myeloid-derived suppressor cells

NK:

Natural killer () cells

NO:

Nitric oxide

NOG:

NOD/Shi-scid/IL-2Rγnull

NSCLC:

Non-small cell lung cancer

OSCC:

Oral squamous cell carcinoma

OS:

Overall survival

PRR:

Pattern recognition receptor

PlGF:

Placenta growth factor

PDGF:

Platelet-derived growth factor

PMN-MDSC:

Polymorphonuclear myeloid- derived suppressor cells

PD-1:

Programmed cell death-1

PSF:

Progression-free survival

ROS:

Reactive oxygen species

RSV:

Respiratory syncytial virus

Siglec-8:

Sialic-binding immunoglobulin like lectin 8

S. aureus :

Staphylococcus aureus

Th2:

T helper 2

TSLP:

Thymic stromal lymphopoietin

TREG:

T regulatory cell

TAM:

Tumor-associated macrophages

TATE:

Tumor-associated tissue eosinophilia

TILs:

Tumor-infiltrating lymphocytes

TME:

Tumor microenvironment

TK:

Tyrosine kinase

VEGF:

Vascular endothelial growth factor

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Acknowledgments

The authors apologize to the many researchers who have contributed importantly to this field and whose work has not been cited due to space and citation restrictions. The authors thank Dr. Gjada Criscuolo for critical reading of the manuscript, scientists from the CISI Laboratory and Schiavoni’s Laboratory not listed as authors for invaluable collaborations to the work reviewed, and medical graphic artist Fabrizio Fiorbianco for preparing Fig. 1.1. This work was supported in part by grants from CISI-Lab Project (University of Naples Federico II), CRèME Project, and TIMING Project (Regione Campania) to G.M. and from AIRC IG 21366 to G.S.

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Mattei, F. et al. (2020). Eosinophils in the Tumor Microenvironment. In: Birbrair, A. (eds) Tumor Microenvironment. Advances in Experimental Medicine and Biology, vol 1273. Springer, Cham. https://doi.org/10.1007/978-3-030-49270-0_1

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