Tumor microenvironment converts plasmacytoid dendritic cells into immunosuppressive/tolerogenic cells: insight into the molecular mechanisms

Journal of Leukocyte Biology

Philippe Delvenne¹  Pascale Hubert¹  Michael Herfs¹  Stéphanie Demoulin¹ 

[1] University of Liege, GIGA-Cancer, Laboratory of Experimental Pathology, Liege, BelgiumUniversity of Liege, GIGA-Cancer, Laboratory of Experimental Pathology, Liege, BelgiumUniversity of Liege, GIGA-Cancer, Laboratory of Experimental Pathology, Liege, Belgium

关键词: antitumor immunity;    cancer;    immunosuppression;   

DOI  :  10.1189/jlb.0812397

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Human pDCs represent a rare population of circulating cells characterized by a rapid and massive TLR-dependent secretion of type I IFN in response to pathogenic agents or danger signals. Through their capacity to bring together innate and adaptive immunity and to secrete soluble factors controlling cancer development, these cells could represent important actors in antitumor immunity. However, accumulating evidence suggests that pDCs recruited to the tumor microenvironment often display a nonactivated state and are associated with the development and maintenance of immunosuppression. Here, we present an overview of neoplastic lesions associated with an infiltration of immunosuppressive/tolerogenic pDC. Moreover, as the proper response of pDC against cancer depends on a critical balance between immune-activating and immune-suppressing mechanisms, we summarize current knowledge about the molecular pathways developed by tumors to prevent antitumoral pDC immune responses. A better understanding of the mechanisms regulating pDC function in tumors could aid in the development of new therapies. Indeed, effective cancer vaccines or therapies could combine immunoactivating strategies (i.e., TLR agonists) with elimination of immune-suppressing mechanisms, leading to pDC reprogramming and thus, allowing tumor rejection in a clinical setting.

【 授权许可】

Unknown