Reprogramming Tumor Associated Macrophages toward M1 Phenotypes with Nanomedicine for Anticancer Immunotherapy. Issue 5 (16th February 2020)

• Record Type: Journal Article
• Authors: Xu, Xiaoxuan; Gong, Xiang; Wang, Yuqi; Li, Jie; Wang, Hong; Wang, Jiaoying; Sha, Xianyi; Li, Yaping; Zhang, Zhiwen
• Is Part Of: Advanced therapeutics. Volume 3:Issue 5(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-02-16
• Subjects: drug delivery -- immunotherapy -- macrophage repolarization -- nanomedicine -- tumor associated macrophages; Therapeutics -- Periodicals; Pharmaceutical technology -- Periodicals; Pharmacogenetics -- Periodicals; 615.5
• DOI: 10.1002/adtp.201900181
• Languages: English
• ISSNs: 2366-3987

Abstract

Abstract: Tumor‐associated macrophages (TAMs), one of the most important constituents in tumor immunosuppressive microenvironments, are a potential therapeutic target due to their essential role in promoting tumor progression and metastasis. Macrophages are usually divided into two categories of protumoral M2‐like TAMs and antitumoral M1 phenotypes at the two extremes. Reprogramming M2‐like TAMs toward tumoricidal M1 phenotype is especially intriguing in terms of the restoration of antitumor immunity for anticancer immunotherapy. In this review, the recent advances of nanomedicine‐mediated reprogramming of TAMs from M2 to M1 to elicit the antitumor immunity are discussed. This reprogramming can be achieved via direct re‐education by targeted delivery of various active agents to TAMs and indirect re‐education by modulating the abnormal tumor microenvironment. Perspectives on nanomedicine mediated TAMs‐M1 reprogramming for effective anticancer immunotherapy are also presented. Abstract : Reprogramming protumoral tumor associated macrophages (TAMs) toward a tumoricidal M1 phenotype is especially intriguing to restore the antitumor immunity for anticancer immunotherapy. Nanomedicine‐mediated TAMs reprogramming can be achieved via direct reprogramming by targeted delivery of various active agents to TAMs and indirect reprogramming by modulating the abnormal tumor microenvironments.