title: Control of IgE and selective T(H)1 and T(H)2 cytokines by PG102 isolated from Actinidia arguta.
abstract: BACKGROUND
  Various allergic responses are thought to result from the unbalanced development of T(H)1 and T(H)2 pathways and, subsequently, the overproduction of IgE. Therefore the modulation of T(H)1 and T(H)2 responses is a rational strategy for the treatment of allergic diseases.
  
  
  OBJECTIVE
  The present study was performed to investigate the immune-modulating activities of PG102 preparations from Actinidia arguta in ovalbumin-sensitized murine models.
  
  
  METHODS
  Two preparations from A arguta, PG102T and PG102E, were chosen for animal experimentation on the basis of their ability to regulate the production of IgE in U266B1 cells. The changes in splenic levels of cytokines and plasma levels of immunoglobulin isotypes were examined. The effects of PG102 on subcellular composition (CD4(+)IL-4(+) or CD19(+)IgE(+) cells), IgE production in B cells, and selective transcription factors were analyzed.
  
  
  RESULTS
  Oral administration of PG102T and PG102E significantly decreased the level of selective T(H)2 cytokines, whereas it increased the level of T(H)1 cytokines. The differential effects of PG102T and PG102E on T(H)1 and T(H)2 cytokines were accompanied by a decrease in the plasma levels of IgE and IgG1 and by an increase in the plasma level of IgG2a. The percentages of both IL-4-producing T cells and IgE-producing B cells were decreased. The concentration of IgE produced within B cells also appeared to be reduced. Finally, PG102T and PG102E downregulated the level of GATA-binding protein 3, while inducing that of T-box transcription factor and nuclear factor of activated T cells c2.
  
  
  CONCLUSIONS
  PG102T and PG102E have great potential as orally active immune modulators for the therapy of various allergic diseases.
authors.affiliation: School of Biological Sciences and Institute of Molecular Biology and Genetics, Seoul National University, Korea.
authors.forename: Eun-Jin
authors.initials: EJ
authors.lastname: Park
authors.forename: Bongcheol
authors.initials: B
authors.lastname: Kim
authors.forename: Haekwan
authors.initials: H
authors.lastname: Eo
authors.forename: Kyungcheol
authors.initials: K
authors.lastname: Park
authors.forename: Yeonran
authors.initials: Y
authors.lastname: Kim
authors.forename: Hwa Jun
authors.initials: HJ
authors.lastname: Lee
authors.forename: Miwon
authors.initials: M
authors.lastname: Son
authors.forename: Yoon-Seok
authors.initials: YS
authors.lastname: Chang
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.forename: Sunyoung
authors.initials: S
authors.lastname: Kim
authors.forename: Mirim
authors.initials: M
authors.lastname: Jin
mesh_terms: D029042:Actinidia / Q000737:chemistry*; D000284:Administration, Oral; D000818:Animals; D001402:B-Lymphocytes / Q000187:drug effects; D045744:Cell Line, Tumor; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005260:Female; D007114:Immunization; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D007132:Immunoglobulin Isotypes / Q000097:blood; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects; D018417:Th1 Cells / Q000187:drug effects / Q000378:metabolism*; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D016207:Cytokines; D007132:Immunoglobulin Isotypes; D008070:Lipopolysaccharides; D010936:Plant Extracts; D014157:Transcription Factors; D007073:Immunoglobulin E; D010047:Ovalbumin