Autoimmune thyroid diseases.
OBJECTIVE
Interesting clinical and basic studies have been published in the field of autoimmune thyroiditis (represented by Graves' disease and Hashimoto's thyroiditis) since January 2005. The review is organized into four main areas: genetics, environment, adaptive immune system, and innate immune system.


RESULTS
The quest continues for the identification of susceptibility genes for autoimmune thyroiditis. In addition to the classical major histocompatibility complex class II genes and cytotoxic T cell antigen-4, new studies have appeared on CD40 the protein tyrosine phosphatase-22. Too much iodine increases the incidence of Hashimoto's thyroiditis, perhaps by augmenting the antigenicity of thyroglobulin. T regulatory cells, Toll-like receptors and presentation of lipid antigens by CD1 molecules are new areas of basic immunological investigation that have been applied to autoimmune thyroiditis.


CONCLUSIONS
Overall, the studies have greatly expanded our understanding of the pathogenesis of thyroiditis. They have opened new lines of investigations that will ultimately result in a better clinical practice.
Caturegli
Patrizio
P
Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA. pcat@jhmi.edu
Kimura
Hiroaki
H
Rocchi
Roberto
R
Rose
Noel R
NR
D000222:Adaptation, Physiological; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D004777:Environment; D006111:Graves Disease / Q000209:etiology / Q000235:genetics / Q000276:immunology; D050031:Hashimoto Disease / Q000209:etiology / Q000235:genetics / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate; D012643:Selenium / Q000172:deficiency; D013967:Thyroiditis, Autoimmune / Q000209:etiology / Q000235:genetics* / Q000276:immunology*
D012643:Selenium