title: Transition of tumor-associated macrophages from MHC class II(hi) to MHC class II(low) mediates tumor progression in mice.
abstract: BACKGROUND
  Tumor-associated macrophages (TAMs) are the most abundant immune cells within the tumor stroma and play a crucial role in tumor development. Although clinical investigations indicate that high levels of macrophage (MΦ) infiltration into tumors are associated with a poor prognosis, the exact role played by TAMs during tumor development remains unclear. The present study aimed to investigate dynamic changes in TAM major histocompatibility complex (MHC) class II expression levels and to assess the effects of these changes on tumor progression.
  
  
  RESULTS
  Significant inhibition of tumor growth in the murine hepatocellular carcinoma Hepa1-6 model was closely associated with partial TAM depletion. Strikingly, two distinct TAM subsets were found to coexist within the tumor microenvironment during Hepa1-6 tumor development. An MHC class II(hi) TAM population appeared during the early phase of tumor development and was associated with tumor suppression; however, an MHC class II(low) TAM population became increasingly predominant as the tumor progressed.
  
  
  CONCLUSIONS
  Tumor progression was positively correlated with increasing infiltration of the tumor tissues by MHC class II(low) TAMs. Thus, targeting the transition of MΦ may be a novel strategy for drug development and immunotherapy.
authors.affiliation: Laboratory of Pathogen Biology, State Key Laboratory of Respiratory Disease, Center for Infection and Immunity, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
authors.forename: Benfan
authors.initials: B
authors.lastname: Wang
authors.forename: Qinyan
authors.initials: Q
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Qin
authors.forename: Siting
authors.initials: S
authors.lastname: Zhao
authors.forename: Jinyan
authors.initials: J
authors.lastname: Wang
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Chen
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D045744:Cell Line, Tumor; D004002:Clodronic Acid / Q000494:pharmacology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000276:immunology / Q000378:metabolism*; D047589:Leukocyte Reduction Procedures; D008081:Liposomes; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism / Q000637:transplantation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009361:Neoplasm Invasiveness / Q000276:immunology; D009369:Neoplasms / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology; D059016:Tumor Microenvironment / Q000276:immunology*
chemical_list: D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D008081:Liposomes; D004002:Clodronic Acid