Th1/Th2-balance in anterior chamber-associated immune deviation by alloantigen

• Published in: Graefe's archive for clinical and experimental ophthalmology Vol. 240; no. 2; pp. 154 - 159
• Main Authors: SAKAI, Rieko, YAMAGAMI, Satoru, INOKI, Taeko, TSURU, Tadahiko, KAWASHIMA, Hidetoshi
• Format: Journal Article
• Language: English
• Published: Berlin Springer 01.02.2002; Springer Nature B.V
• Subjects: Animals; Anterior Chamber - immunology; Biological and medical sciences; Cytokines - genetics; Cytokines - metabolism; Enzyme-Linked Immunosorbent Assay; Hypersensitivity, Delayed - immunology; Isoantigens - immunology; Male; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Miscellaneous; Ophthalmology; Spleen - immunology; Th1 Cells - immunology; Th2 Cells - immunology; Immune response; Rodentia; Cytokine; Th1 lymphocyte; Experimental study; Vertebrata; Mammalia; Alloantigen; Mouse; Animal; Anterior chamber; Immune deviation; Th2 lymphocyte
• ISSN: 0721-832X; 1435-702X
• DOI: 10.1007/s00417-001-0422-2

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. 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. 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. 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.