Invariant NKT Cell Lines Derived from the NOD·H2h4Mouse Enhance Autoimmune Thyroiditis

Author:

Sharma Rajni B.1,Fan Xiaoguang1,Caturegli Patrizio1,Rose Noel R.12,Burek C. Lynne12

Affiliation:

1. Department of Pathology, School of Medicine, Bloomberg School of Public Health, Johns Hopkins Medical Institutions, Johns Hopkins University, Ross Research Building, 648, 720 Rutland Avenue, Baltimore, MD 21205, USA

2. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins Medical Institutions, Johns Hopkins University, Ross Research Building, 648, 720 Rutland Avenue, Baltimore, MD 21205, USA

Abstract

To study the role of invariant Natural Killer T cell (iNKT) cells in autoimmune thyroiditis, we derived two iNKT cell lines from the spleens of NOD·H2h4mice, a strain that develops spontaneous autoimmune thyroiditis exacerbated by excess dietary iodine. The two lines were CD1d-restricted and expressed CD4+, DX5+, and the Vα4Jα281 gene segment, of the T-cell receptor α locus. Upon stimulation with α-galactosyl-ceramide (α-GalCer), both lines rapidly produced IL-2, IL-4, IFN-γ, IL-10, and TNF-α. Strikingly, a similar cytokine response was also induced by thyroglobulin, one of the most abundant protein in the thyroid gland and a major autoantigen in human autoimmune thyroiditis. Transfer of the iNKT cell lines to syngeneic hosts enhanced autoimmune thyroiditis. Intraperitoneal injections of α-GalCer in iodine primed mice also induced thyroid disease. This paper reports for the first time that iNKT cells respond to thyroglobulin and enhance autoimmune thyroiditis in iodine fed NOD·H2h4mice.

Funder

Department of Immunology, The Scripps Research Institute, La Jolla

Publisher

Hindawi Limited

Subject

Endocrinology, Diabetes and Metabolism

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