title: Improved Anti-Treg Vaccination Targeting Foxp3 Efficiently Decreases Regulatory T Cells in Mice.
abstract: The critical role of regulatory T (Treg) cells in dampening immune responses against tumor cells is apparent. Therefore, several methods have been introduced for eliminating Treg. Among them, inducing immune responses against Treg cells expressing Foxp3 transcription factor is a hopeful approach to decrease the frequency of Tregs. In current study, we used the chimeric FoxP3-Fc(IgG) fusion construct/protein to effectively stimulate the immune responses against Treg cells.
  
  
  
  Previously constructed FoxP3-Fc(IgG) DNA vaccine and its protein counterpart were injected into C57BL/6 mice in a prime/boost regimen. After 2 weeks, the mice were killed to measure the frequency of Tregs in their spleens, as well as analyze their specific cytokine production, T-cell proliferation, and CD8 T-cell cytotoxicity against FoxP3 protein.
  
  
  
  FACS analysis of FoxP3 CD4 cells in splenocytes revealed the efficiency of FoxP3 DNA-prime protein-boost strategy to decrease the Treg cells and further showed considerable superiority of Fc(IgG) fusion strategy. This significant reduction in Treg frequency was also concomitant with higher FoxP3-specific CTL and Th1 responses in FoxP3-Fc vaccinated animals.
  
  
  
  Prime/boost vaccination against FoxP3 in addition to enhanced antigen presentation by means of Fc fusion strategy could be successfully considered for Treg depletion studies. Validity of this approach should be experimentally tested in preclinical tumor models.
authors.affiliation: *Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz Departments of †Hepatitis and AIDS ‡Immunology, Pasteur Institute of Iran Departments of §Immunology, School of Medicine ∥Molecular Medicine, School of Advanced Technologies in Medicine #Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran ¶Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
authors.forename: Neda
authors.initials: N
authors.lastname: Mousavi Niri
authors.forename: Arash
authors.initials: A
authors.lastname: Memarnejadian
authors.forename: Younes
authors.initials: Y
authors.lastname: Pilehvar-Soltanahmadi
authors.forename: Mohammadreza
authors.initials: M
authors.lastname: Agha Sadeghi
authors.forename: Mehdi
authors.initials: M
authors.lastname: Mahdavi
authors.forename: Nasim
authors.initials: N
authors.lastname: Kheshtchin
authors.forename: Samaneh
authors.initials: S
authors.lastname: Arab
authors.forename: Afshin
authors.initials: A
authors.lastname: Namdar
authors.forename: Farhad
authors.initials: F
authors.lastname: Jadidi
authors.forename: Nosratollah
authors.initials: N
authors.lastname: Zarghami
authors.forename: Jamshid
authors.initials: J
authors.lastname: Hajati
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D019496:Cancer Vaccines / Q000276:immunology*; D002478:Cells, Cultured; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism*; D007141:Immunoglobulin Fc Fragments / Q000235:genetics; D008212:Lymphocyte Depletion; D051379:Mice; D008810:Mice, Inbred C57BL; D009369:Neoplasms / Q000276:immunology / Q000628:therapy*; D011993:Recombinant Fusion Proteins / Q000235:genetics; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D014611:Vaccination; D019444:Vaccines, DNA
chemical_list: D019496:Cancer Vaccines; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D007141:Immunoglobulin Fc Fragments; D011993:Recombinant Fusion Proteins; D019444:Vaccines, DNA