Autoimmune thyroid disease and thyroid cell class II major histocompatibility complex antigens.
Autoimmune thyroid disease and thyroid cell class II major histocompatibility complex antigens.
复制标题
自身免疫性甲状腺疾病和甲状腺细胞 II 类主要组织相容性复合体抗原。
DOI:
10.1111/j.1365-2265.1987.tb00783.x
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发表时间:
1987
影响因子:
3.2
通讯作者:
Davies,TF
中科院分区:
文献类型:
--
作者:
Piccinini,LA;Roman,SH;Davies,TF
Differences in the immune response to antigenic stimuli, including thyroid autoantigens, have been linked to a group of genes known collectively as the Major Histocompatibility Complex (MHC), which in humans is referred to as the Human Leukocyte Antigen (HLA) complex (Benacerraf, 1981). These genes encode a series of polymorphic cell surface molecules; the class I, 11 & I11 antigens. Classically, class I antigens are expressed on all nucleated cells in the body and are recognized by cytotoxic and suppressor T cells. Class I1 antigens, however, are primarily restricted in their constitutive expression to cells of the immune system and are recognized by the T helper cell subset. Class I11 antigens represent components of the complement pathway. Theories on the aetiology of autoimmune thyroid disease have often invoked a ‘thyroid component’to such immune responses, but the evidence has been indirect and usually in the form of inherited metabolic abnormalities present in the thyroid cell rather than an immunologically-defined antigen (Wick et al., 1982). However, recent studies on intrathyroidal lymphocyte function have demonstrated the potent role of thyroid antigenic stimulation within the target organ (Totterman et al., 1979; McLachlan et al., 1983; Londei et al., 1984). The finding of MHC class I1 antigens on the surface of the murine thyroid cell (Salamero et al., 1981), and later in human thyroid epithelium (Hanafusa et al., 1983), has focused attention on the generalized facilitation by MHC class I1 antigens in the development of thyroid autoimmunity. This review includes a basic introduction to the class I1 antigens and discusses our present understanding of their involvement in the development of human thyroid autoimmunity.