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Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect?

Standard

Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect? / Sospedra, M; Obiols, G; Babi, L F; Tolosa, E; Vargas, F; Roura-Mir, C; Lucas-Martin, A; Ercilla, G; Pujol-Borrell, R.

in: J IMMUNOL, Jahrgang 154, Nr. 8, 15.04.1995, S. 4213-22.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Sospedra, M, Obiols, G, Babi, LF, Tolosa, E, Vargas, F, Roura-Mir, C, Lucas-Martin, A, Ercilla, G & Pujol-Borrell, R 1995, 'Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect?', J IMMUNOL, Jg. 154, Nr. 8, S. 4213-22.

APA

Sospedra, M., Obiols, G., Babi, L. F., Tolosa, E., Vargas, F., Roura-Mir, C., Lucas-Martin, A., Ercilla, G., & Pujol-Borrell, R. (1995). Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect? J IMMUNOL, 154(8), 4213-22.

Vancouver

Sospedra M, Obiols G, Babi LF, Tolosa E, Vargas F, Roura-Mir C et al. Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect? J IMMUNOL. 1995 Apr 15;154(8):4213-22.

Bibtex

@article{092fc00d2f49497dbeaef9893cfbd731,
title = "Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect?",
abstract = "Thyroid follicular cells (thyrocytes) from Graves' disease (GD) patients' thyroid glands express HLA class II molecules {"}ectopically.{"} This phenomenon has been attributed to induction by locally produced cytokines and may be relevant to disease pathogenesis. We have compared IFN-gamma-mediated induction of HLA class II in thyrocytes from glands affected with GD and a nonautoimmune disease (MNG), to investigate a possible differential regulation of HLA expression between these two pathologies. HLA induction has been measured in primary thyrocyte cultures and control autologous macrophages stimulated or not stimulated with IFN-gamma. Comparison of flow cytometric data using an improved algorithm demonstrated that expression of HLA class II molecules is more readily induced in thyrocytes from GD than from MNG thyroid glands. This higher inducibility was parallel to a faster and stronger induction of 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 of lymphocytic infiltration of the gland. There was no association with a particular HLA class II allele or with the presence of IFN-gamma and IL-2 in the tissue, as assessed by reverse transcription-PCR. No differences in the induction of class II were found in macrophages from each group of patients. These results suggest that an intrinsic feature of thyrocytes from GD patients is an up-regulation of HLA class II expression and that this is a characteristic that may facilitate the triggering of autoimmunity to {"}hyperinducible{"} thyroid glands.",
keywords = "Adolescent, Adult, Aged, Base Sequence, Child, DNA Primers, Female, Gene Expression, Genes, MHC Class II, Goiter, Nodular, Graves Disease, HLA-D Antigens, Haplotypes, Humans, Interferon-gamma, Macrophages, Male, Middle Aged, Molecular Sequence Data, RNA, Messenger, Thyroid Gland",
author = "M Sospedra and G Obiols and Babi, {L F} and E Tolosa and F Vargas and C Roura-Mir and A Lucas-Martin and G Ercilla and R Pujol-Borrell",
year = "1995",
month = apr,
day = "15",
language = "English",
volume = "154",
pages = "4213--22",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "8",

}

RIS

TY - JOUR

T1 - Hyperinducibility of HLA class II expression of thyroid follicular cells from Graves' disease. A primary defect?

AU - Sospedra, M

AU - Obiols, G

AU - Babi, L F

AU - Tolosa, E

AU - Vargas, F

AU - Roura-Mir, C

AU - Lucas-Martin, A

AU - Ercilla, G

AU - Pujol-Borrell, R

PY - 1995/4/15

Y1 - 1995/4/15

N2 - Thyroid follicular cells (thyrocytes) from Graves' disease (GD) patients' thyroid glands express HLA class II molecules "ectopically." This phenomenon has been attributed to induction by locally produced cytokines and may be relevant to disease pathogenesis. We have compared IFN-gamma-mediated induction of HLA class II in thyrocytes from glands affected with GD and a nonautoimmune disease (MNG), to investigate a possible differential regulation of HLA expression between these two pathologies. HLA induction has been measured in primary thyrocyte cultures and control autologous macrophages stimulated or not stimulated with IFN-gamma. Comparison of flow cytometric data using an improved algorithm demonstrated that expression of HLA class II molecules is more readily induced in thyrocytes from GD than from MNG thyroid glands. This higher inducibility was parallel to a faster and stronger induction of 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 of lymphocytic infiltration of the gland. There was no association with a particular HLA class II allele or with the presence of IFN-gamma and IL-2 in the tissue, as assessed by reverse transcription-PCR. No differences in the induction of class II were found in macrophages from each group of patients. These results suggest that an intrinsic feature of thyrocytes from GD patients is an up-regulation of HLA class II expression and that this is a characteristic that may facilitate the triggering of autoimmunity to "hyperinducible" thyroid glands.

AB - Thyroid follicular cells (thyrocytes) from Graves' disease (GD) patients' thyroid glands express HLA class II molecules "ectopically." This phenomenon has been attributed to induction by locally produced cytokines and may be relevant to disease pathogenesis. We have compared IFN-gamma-mediated induction of HLA class II in thyrocytes from glands affected with GD and a nonautoimmune disease (MNG), to investigate a possible differential regulation of HLA expression between these two pathologies. HLA induction has been measured in primary thyrocyte cultures and control autologous macrophages stimulated or not stimulated with IFN-gamma. Comparison of flow cytometric data using an improved algorithm demonstrated that expression of HLA class II molecules is more readily induced in thyrocytes from GD than from MNG thyroid glands. This higher inducibility was parallel to a faster and stronger induction of 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 of lymphocytic infiltration of the gland. There was no association with a particular HLA class II allele or with the presence of IFN-gamma and IL-2 in the tissue, as assessed by reverse transcription-PCR. No differences in the induction of class II were found in macrophages from each group of patients. These results suggest that an intrinsic feature of thyrocytes from GD patients is an up-regulation of HLA class II expression and that this is a characteristic that may facilitate the triggering of autoimmunity to "hyperinducible" thyroid glands.

KW - Adolescent

KW - Adult

KW - Aged

KW - Base Sequence

KW - Child

KW - DNA Primers

KW - Female

KW - Gene Expression

KW - Genes, MHC Class II

KW - Goiter, Nodular

KW - Graves Disease

KW - HLA-D Antigens

KW - Haplotypes

KW - Humans

KW - Interferon-gamma

KW - Macrophages

KW - Male

KW - Middle Aged

KW - Molecular Sequence Data

KW - RNA, Messenger

KW - Thyroid Gland

M3 - SCORING: Journal article

C2 - 7706756

VL - 154

SP - 4213

EP - 4222

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 8

ER -