Shukkur M Farooq1, Hossam M Ashour. 1. Department of Pharmacy Practice, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI 48201, USA.
Abstract
AIMS: Administration of antigens into the anterior chamber (AC) of the eye induces a form of antigen-specific immune tolerance termed anterior chamber-associated immune deviation (ACAID). This immune tolerance effectively impairs host delayed-type hypersensitivity (DTH) responses. We hypothesized that ACAID could be generated in BALB/c mice following AC inoculation of the encephalitogenic antigens myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP). METHODS: We used DTH assays and local adoptive transfer (LAT) assays to test whether MOG/MBP-induced ACAID following their administration into the AC, whether they elicited this immune tolerance via CD8(+) T cells, and whether their AC coadministration (MOG/MBP) induced specific immune tolerance to one or both antigens. RESULTS: We showed that MOG/MBP-induced AC-mediated specific immune tolerance, as evident from impaired DTH responses. This antigen-driven DTH suppression was solely mediated via splenic CD8(+) T cells as confirmed by LAT assays. Finally, a single AC injection with both antigens was sufficient to induce specific immune tolerance to these antigens, as evident from DTH and LAT assays. CONCLUSION: ACAID T-cell regulation could be used as a therapeutic tool in the treatment of complicated autoimmune diseases that involve multiple antigens such as multiple sclerosis.
AIMS: Administration of antigens into the anterior chamber (AC) of the eye induces a form of antigen-specific immune tolerance termed anterior chamber-associated immune deviation (ACAID). This immune tolerance effectively impairs host delayed-type hypersensitivity (DTH) responses. We hypothesized that ACAID could be generated in BALB/c mice following AC inoculation of the encephalitogenic antigens myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP). METHODS: We used DTH assays and local adoptive transfer (LAT) assays to test whether MOG/MBP-induced ACAID following their administration into the AC, whether they elicited this immune tolerance via CD8(+) T cells, and whether their AC coadministration (MOG/MBP) induced specific immune tolerance to one or both antigens. RESULTS: We showed that MOG/MBP-induced AC-mediated specific immune tolerance, as evident from impaired DTH responses. This antigen-driven DTH suppression was solely mediated via splenic CD8(+) T cells as confirmed by LAT assays. Finally, a single AC injection with both antigens was sufficient to induce specific immune tolerance to these antigens, as evident from DTH and LAT assays. CONCLUSION: ACAID T-cell regulation could be used as a therapeutic tool in the treatment of complicated autoimmune diseases that involve multiple antigens such as multiple sclerosis.
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