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2015 ; 64
(ä): 82-90
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Immunogenetics of autoimmune thyroid diseases: A comprehensive review
#MMPMID26235382
Lee HJ
; Li CW
; Hammerstad SS
; Stefan M
; Tomer Y
J Autoimmun
2015[Nov]; 64
(ä): 82-90
PMID26235382
show ga
Both environmental and genetic triggers factor into the etiology of autoimmune
thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's
thyroiditis (HT). Although the exact pathogenesis and causative interaction
between environment and genes are unknown, GD and HT share similar
immune-mediated mechanisms of disease. They both are characterized by the
production of thyroid autoantibodies and by thyroidal lymphocytic infiltration,
despite being clinically distinct entities with thyrotoxicosis in GD and
hypothyroidism in HT. Family and population studies confirm the strong genetic
influence and inheritability in the development of AITD. AITD susceptibility
genes can be categorized as either thyroid specific (Tg, TSHR) or
immune-modulating (FOXP3, CD25, CD40, CTLA-4, HLA), with HLA-DR3 carrying the
highest risk. Of the AITD susceptibility genes, FOXP3 and CD25 play critical
roles in the establishment of peripheral tolerance while CD40, CTLA-4, and the
HLA genes are pivotal for T lymphocyte activation and antigen presentation.
Polymorphisms in these immune-modulating genes, in particular, significantly
contribute to the predisposition for GD, HT and, unsurprisingly, other autoimmune
diseases. Emerging evidence suggests that single nucleotide polymorphisms (SNPs)
in the immunoregulatory genes may functionally hinder the proper development of
central and peripheral tolerance and alter T cell interactions with antigen
presenting cells (APCs) in the immunological synapse. Thus, susceptibility genes
for AITD contribute directly to the key mechanism underlying the development of
organ-specific autoimmunity, namely the breakdown in self-tolerance. Here we
review the major immune-modulating genes that are associated with AITD and their
potential functional effects on thyroidal immune dysregulation.
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