Ontology type: schema:ScholarlyArticle
2002-02
AUTHORSRieko Sakai, Satoru Yamagami, Taeko Inoki, Tadahiko Tsuru, Hidetoshi Kawashima
ABSTRACTBACKGROUND: 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. CONCLUSION: 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. More... »
PAGES154-159
http://scigraph.springernature.com/pub.10.1007/s00417-001-0422-2
DOIhttp://dx.doi.org/10.1007/s00417-001-0422-2
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/11931082
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