Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 105, Issue 10, Pages 1465-1472Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI9213
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Funding
- NIAID NIH HHS [AI-42376] Funding Source: Medline
- NINDS NIH HHS [R01 NS023444, NS-23221, R01 NS023221, NS-23444] Funding Source: Medline
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Transgenic mice expressing the BV8S2 chain, which is specific for the myelin basic protein determinant Ac1-11, possess a naturally induced set of regulatory T cells directed against BV8S2. Further activation of anti-BV8S2 T cells in male mice with recombinant BV8S2 protein can inhibit IFN-gamma release by Ac1-11-specific T cells through a cytokine-driven mechanism and prevent induction of experimental autoimmune encephalomyelitis (EAE). In contrast, naive female mice possess fewer anti-BV8S2-reactive T cells, and treatment with BV8S2 delayed but did not prevent EAE. We here demonstrate that combining T-cell receptor (TCR) vaccination with supplemental estrus doses of estrogen potentiated IL-10 production by anti-BV8S2-reactive T cells and induced Ac1-11-specific T cells to produce IL-10 and TGF-beta. This combined treatment resulted in full protection against EAE, which was not observed with either therapy alone. These findings imply that supplemental estrogen can enhance the efficacy of TCR-based immunotherapy for autoimmune diseases that predominate in females.
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