In vivo evidence for CD4+ and CD8+ suppressor T cells in vaccination-induced suppression of murine experimental autoimmune thyroiditis

Journal Article · Sun Sep 01 04:00:00 EDT 1991 · Clinical Immunology and Immunopathology; (United States)

DOI:https://doi.org/10.1016/0090-1229(91)90103-H· OSTI ID:5227135

Flynn, J C; Kong, Y C ^[1]

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1. Wayne State University School of Medicine, Detroit, Michigan (USA)

In several experimental autoimmune diseases, including experimental autoimmune thyroiditis (EAT), vaccination with attenuated autoantigen-specific T cells has provided protection against subsequent induction of disease. However, the mechanism(s) of vaccination-induced suppression remains to be clarified. Since the authors have previously shown that suppression generated by pretreatment with mouse thyroglobulin (MTg) or thyroid-stimulating hormone in EAT is mediated by CD4+, not CD8+, suppressor T cells, they examined the role of T cell subsets in vaccination-induced suppression of EAT. Mice were vaccinated with irradiated, MTg-primed, and MTg-activated spleen cells and then challenged. Pretreatment with these cells suppressed EAT induced by immunization with MTg and adjuvant, but not by adoptive transfer of thyroiditogenic cells, suggesting a mechanism of afferent suppression. The activation of suppressor mechanisms did not require CD8+ cells, since mice depleted of CD8+ cells before vaccination showed reduced EAT comparable to control vaccinated mice. Furthermore, depletion of either the CD4+ or the CD8+ subset after vaccination did not significantly abrogate suppression. However, suppression was eliminated by the depletion of both CD4+ and CD8+ cells in vaccinated mice. These results provide evidence for the cooperative effects of CD4+ and CD8+ T cells in vaccination-induced suppression of EAT.

• OSTI ID: 5227135
• Journal Information: Clinical Immunology and Immunopathology; (United States), Journal Name: Clinical Immunology and Immunopathology; (United States) Vol. 60:3; ISSN CLIIA; ISSN 0090-1229
• Country of Publication: United States
• Language: English

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