Journal
CELLULAR IMMUNOLOGY
Volume 226, Issue 1, Pages 20-29Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2003.11.002
Keywords
experimental autoimmune thyroiditis; autoimmunity; regulatory T cells; CD25; CD137; 4-1BB
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Funding
- NCI NIH HHS [CA-79915] Funding Source: Medline
- NIDDK NIH HHS [DK-45960] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA079915] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK045960] Funding Source: NIH RePORTER
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Experimental autoimmune thyroiditis (EAT), a model for Hashimoto's thyroiditis, is a T cell-mediated disease inducible with mouse thyroglobulin (mTg). Pretreatment with mTg, however, can induce CD4(+) T cell-mediated tolerance to EAT. We demonstrate that CD4(+)CD25(+) regulatory cells are critical for the tolerance induction, as in vivo depletion of CD25(+) cells abrogated established tolerance, and CD4(+)CD25(+) cells from tolerized mice suppressed mTg-responsive cells in vitro. Importantly, administration of an agonistic CD137 monoclonal antibody (mAb) inhibited tolerance development, and the mediation of established tolerance. CD137 mAb also inhibited the suppression of mTg-responsive cells by CD4(+)CD25(+) cells in vitro. Signaling through CD137 likely resulted in enhancement of the responding inflammatory T cells, as anti-CD137 did not enable CD4(+)CD25(+) T cells to proliferate in response to mTg in vitro. (C) 2003 Elsevier Inc. All rights reserved.
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