title: Interleukin 10 and transforming growth factor beta contribute to the development of experimentally induced allergic conjunctivitis in mice during the effector phase.
abstract: OBJECTIVE
  To investigate the involvement of interleukin (IL)10 and transforming growth factor (TGF) beta in the development of experimentally induced allergic conjunctivitis in mice.
  
  
  METHODS
  Balb/c mice were actively sensitised with ragweed in alum, and then challenged with ragweed in eye drops after 10 days. 24 h later, the conjunctivas, spleens and blood were collected for histological and cytokine expression analyses, proliferation and cytokine production assays and measurement of immunoglobulin (Ig) levels. Mice developing experimentally induced allergic conjunctivitis were injected intraperitoneally with 200 microg of anti-IL10 or anti-TGF beta antibodies at 0, 2, 4, 6 and 8 days (induction phase treatment) or 500 microg of antibodies 2 h before ragweed challenge (effector phase treatment). Normal rat IgG was used for control injections.
  
  
  RESULTS
  Treatment with either anti-IL10 or anti-TGF beta antibodies during the induction phase did not affect eosinophil infiltration into the conjunctiva. By contrast, treatment with either antibody during the effector phase suppressed infiltration. During the effector phase, treatment with anti-TGF beta antibody, but not the anti-IL10 antibody, markedly up regulated proliferation and Th2 cytokine production by splenocytes. IL1alpha levels in the conjunctiva were reduced after treatment with either antibody; in addition, eotaxin and tumour necrosis factor alpha levels were reduced after treatment with antibody to TGF beta.
  
  
  CONCLUSIONS
  IL10 and TGF beta do not have immunosuppressive roles in the development of experimentally induced allergic conjunctivitis. Rather, they augment the infiltration of eosinophils into the conjunctiva during the effector phase of experimentally induced allergic conjunctivitis.
authors.affiliation: Department of Ophthalmology and Visual Science, Kochi Medical School, Kohasu, Nankoku, Japan. fukusima@med.kochi-u.ac.jp
authors.forename: A
authors.initials: A
authors.lastname: Fukushima
authors.forename: T
authors.initials: T
authors.lastname: Sumi
authors.forename: K
authors.initials: K
authors.lastname: Fukuda
authors.forename: N
authors.initials: N
authors.lastname: Kumagai
authors.forename: T
authors.initials: T
authors.lastname: Nishida
authors.forename: H
authors.initials: H
authors.lastname: Yagita
authors.forename: H
authors.initials: H
authors.lastname: Ueno
mesh_terms: D019264:Adoptive Transfer; D031164:Ambrosia / Q000276:immunology; D000818:Animals; D049109:Cell Proliferation; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D003228:Conjunctiva / Q000276:immunology; D003233:Conjunctivitis, Allergic / Q000276:immunology* / Q000473:pathology; D004802:Eosinophilia / Q000276:immunology; D005260:Female; D016753:Interleukin-10 / Q000276:immunology*; D053582:Interleukin-1alpha / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013154:Spleen / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: C515457:Ccl11 protein, mouse; C515458:Ccl11 protein, rat; D054413:Chemokine CCL11; D019742:Chemokines, CC; D053582:Interleukin-1alpha; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10