IMR Press / FBL / Volume 25 / Issue 2 / DOI: 10.2741/4804

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Homology between TSH-R/Tg/TPO and Hashimoto’s encephalopathy autoantigens
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1 Department of Clinical and Experimental Medicine - Endocrinology, University of Messina, via Consolare Valeria - Gazzi, 98125 Messina, Italy
2 Master Program on Childhood, Adolescent and Women’s Endocrine Health, University of Messina, via Consolare Valeria - Gazzi, 98125 Messina, Italy
3 Interdepartmental Program on Molecular and Clinical Endocrinology and Women’s Endocrine Health, AOU Policlinico G. Martino, via Consolare Valeria - Gazzi, 98125 Messina, Italy
4 Department of Clinical and Experimental Medicine - Dermatology, University of Messina, via Consolare Valeria - Gazzi, 98125 Messina, Italy
Send correspondence to: Fabrizio Guarneri, Department of Clinical and Experimental Medicine, Dermatology, via Consolare Valeria, Gazzi, 98125 Messina, Italy, Tel: 39 090 2212890, Fax: 39 090 2927691, E-mail: f.guarneri@tiscali.it
Front. Biosci. (Landmark Ed) 2020, 25(2), 229–241; https://doi.org/10.2741/4804
Published: 1 January 2020
Abstract

Hashimoto’s encephalopathy (HE) is a syndrome occurring in some patients with Hashimoto’s thyroiditis or, less frequently, Graves’ disease. Three known autoantigens are involved in HE: alpha-enolase, dimethylargininase-I (DDAHI) and aldehyde reductase-I (AKRIAI). We searched for amino acid sequence homologies between these proteins and the three classical thyroid autoantigens (thyroperoxidase (TPO), thyroglobulin (Tg), TSH-receptor (TSH-R)), which are also expressed in the central nervous system (CNS). TSH-R shows homologies with alpha-enolase (n=4), DDAHI (n=2) and AKRIAI (n=5); of these segments, two, two and four, respectively, overlap totally or partially with epitope-containing TSH-R segments. Tg has 10 homologies with alpha-enolase, five with DDAHI, and eight with AKRIAI; epitope-containing segments of Tg overlap four, three and four segments, respectively. TPO has six segments homologous to alpha-enolase, three to DDAHI and seven to AKRIAI; of these segments, five, one and four, respectively, are located in epitope-containing parts. These data suggest that cross-reactivity between CNS autoantigens and thyroid autoantigens might contribute to the HE pathogenesis, together with other proposed mechanisms, including autoimmunity involving autoantigens common to CNS and thyroid.

Keywords
Hashimoto’s encephalopathy
Autoimmunity
Thyroid
Brain
Central nervous system
Molecular mimicry
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