HYPERINDUCIBILITY OF HLA CLASS-II EXPRESSION OF THYROID FOLLICULAR CELLS FROM GRAVES-DISEASE - A PRIMARY DEFECT

Citation
M. Sospedra et al., HYPERINDUCIBILITY OF HLA CLASS-II EXPRESSION OF THYROID FOLLICULAR CELLS FROM GRAVES-DISEASE - A PRIMARY DEFECT, The Journal of immunology, 154(8), 1995, pp. 4213-4222
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
0022-1767 → ACNP
Volume
154
Issue
8
Year of publication
1995
Pages
4213 - 4222
Database
ISI
SICI code
0022-1767(1995)154:8<4213:HOHCEO>2.0.ZU;2-7
Abstract
Thyroid follicular cells (thyrocytes) from Graves' disease (GD) patien ts' thyroid glands express HLA class II molecules ''ectopically.'' Thi s phenomenon has been attributed to induction by locally produced cyto kines and may be relevant to disease pathogenesis. We have compared IF N-gamma-mediated induction of HLA class II in thyrocytes from glands a ffected with GD and a nonautoimmune disease (MNG), to investigate a po ssible differential regulation of HLA expression between these two pat hologies. HLA induction has been measured in primary thyrocyte culture s and control autologous macrophages stimulated or not stimulated with IFN-gamma. Comparison of flow cytometric data using an improved algor ithm demonstrated that expression of HLA class II molecules is more re adily induced in thyrocytes from GD than from MNG thyroid glands. This higher inducibility was parallel to a faster and stronger induction o f HLA class II message in GD thyrocytes but did not correlate with the levels of. HLA class II or class I originally expressed by thyrocytes in the tissue or with the degree oi lymphocytic infiltration of the g land. There was no association with a particular HLA class II allele o r with the presence of IFN-gamma and IL-2 in the tissue, as assessed b y reverse transcription-PCR. No differences in the induction of class II were found in macrophages from each group of patients. These result s suggest that an intrinsic feature of thyrocytes from GD patients is an up-regulation of HLA class II expression and that this is a charact eristic that may facilitate the triggering of autoimmunity to ''hyperi nducible'' thyroid glands.