title: Th1/Th2-balance in anterior chamber-associated immune deviation by alloantigen.
abstract: BACKGROUND
  Immune deviation induced by an injection of antigens (Ags) in the anterior chamber of the eye has been termed anterior chamber-associated immune deviation (ACAID). Inoculated Ag induces the generation of T cells that down-regulate delayed-type hypersensitivity (DTH). The induction mechanism may well involve various cytokines.
  
  
  METHODS
  BALB/c mice were inoculated with C3H/He splenocytes. After a week, subcutaneous immunization was performed in mice with (ACAID group) or without (positive control group) intracameral inoculation of splenocytes. DTH responses were determined by ear-swelling assay a week after subcutaneous immunization. To ascertain which cytokines suppress or promote ACAID induction, the gene transcription levels of various cytokines were evaluated by ribonuclease protection assay in alloantigen-pulsed splenocytes. Enzyme-linked immunosorbent assay was performed to quantitate cytokine production in the culture supernatants.
  
  
  RESULTS
  Alloantigen-specific DTH was suppressed in the ACAID group. Interleukin (IL)-2 and interferon-gamma (IFN-gamma) gene transcription levels in the ACAID-induced group were significantly suppressed, but IL-4, IL-5, IL-6, IL-9, and IL-10 gene transcription levels were not different from those in the positive control group. IFN-gamma and IL-2 production in the ACAID group was significantly suppressed compared with that in the positive control group. Increased expression of IL-4 and IL-10 was not detected in the ACAID group compared with the positive control group.
  
  
  CONCLUSIONS
  The results suggest that Th1 suppression of cytokine secretion in the splenic phase plays a role in ACAID induction and Th2-secreting cytokines do not particularly affect ACAID induction by alloantigen.
authors.affiliation: Department of Ophthalmology, Jichi Medical School, Minamikawachi, Tochigi, Japan.
authors.forename: Rieko
authors.initials: R
authors.lastname: Sakai
authors.forename: Satoru
authors.initials: S
authors.lastname: Yamagami
authors.forename: Taeko
authors.initials: T
authors.lastname: Inoki
authors.forename: Tadahiko
authors.initials: T
authors.lastname: Tsuru
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Kawashima
mesh_terms: D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007519:Isoantigens / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D013154:Spleen / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D007519:Isoantigens