IL13-Mediated Dectin-1 and Mannose Receptor Overexpression Promotes Macrophage Antitumor Activities through Recognition of Sialylated Tumor Cells.

Abstract:

:Macrophage-mediated cytotoxicity is controlled by surface receptor expression and activation. Despite the numerous studies documenting the role of macrophage C-type lectin receptors (CLR) in pathogen elimination, little is known about their contribution to antitumor responses. Here, we report that IL13 inhibits T-cell lymphoma and ovarian adenocarcinoma development in tumor-bearing mice through the conversion of tumor-supporting macrophages to cytotoxic effectors, characterized by a CLR signature composed of dectin-1 and mannose receptor (MR). We show that dectin-1 and MR are critical for the recognition of tumor cells through sialic acid-specific glycan structure on their surface and for the subsequent activation of macrophage tumoricidal response. Finally, we validated that IL13 antitumor effect mediated by dectin-1 and MR overexpression on macrophages can extend to various types of human tumors. Therefore, these results identify these CLRs as potential targets to promote macrophage antitumor response and represent an attractive approach to elicit tumor-associated macrophage tumoricidal properties.

journal_name

Cancer Immunol Res

authors

Alaeddine M,Prat M,Poinsot V,Gouazé-Andersson V,Authier H,Meunier E,Lefèvre L,Alric C,Dardenne C,Bernad J,Alric L,Segui B,Balard P,Couderc F,Couderc B,Pipy B,Coste A

doi

10.1158/2326-6066.CIR-18-0213

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

321-334

issue

2

eissn

2326-6066

issn

2326-6074

pii

2326-6066.CIR-18-0213

journal_volume

7

pub_type

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