Open Access
Review

The autoimmunity in Graves's disease

Hong Li1,*,Tao Wang1
1
Department of Endocrinology, Long Hua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, P.R. China
DOI: 10.2741/4141 Volume 18 Issue 2, pp.782-787
Published: 01 January 2013
(This article belongs to the Special Issue Cellular immunology and stem cell biology)
*Corresponding Author(s):  
Hong Li
E-mail:  
shanhongli2012@yeah.net
Abstract

Graves’ disease (GD) is a systemic autoimmune syndrome manifesting complications in thyroid and orbital connective tissues. The thyroid gland plays a major role in the human body by producing the hormones necessary for appropriate energy levels and an active life. At the same time, the thyroid is highly vulnerable to autoimmune thyroid diseases. GD arises due to the complex interplay of genetic, environmental and endogenous factors, and the specific combination is required to initiate thyroid autoimmunity. Earlier studies have demonstrated the autoimmune response plays a dominant role in the development of GD. This review summarizes the inflammatory events which occur during the development of GD, such as Th17/Treg cell infiltration, Th1/Th2 cytokine and chemokine production, and the subtypes of immunogloblins (IgGs) generated.

Key words

Graves' disease, IFN–gamma, IL-2, Review

Share and Cite
Hong Li, Tao Wang. The autoimmunity in Graves's disease. Frontiers in Bioscience-Landmark. 2013. 18(2); 782-787.