Fas-FasL in Hashimoto's thyroiditis

G. Stassi, A. Zeuner, D. Di Liberto, M. Todaro, L. Ricci-Vitiani, R. De Maria

Research output: Contribution to journalArticle

Abstract

Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.

Original languageEnglish
Pages (from-to)19-23
Number of pages5
JournalJournal of Clinical Immunology
Volume21
Issue number1
DOIs
Publication statusPublished - 2001

Fingerprint

Hashimoto Disease
Hypothyroidism
Autoimmunity
Autoimmune Diseases
Fibrosis
Chronic Disease
Clone Cells
Thyroid Epithelial Cells
T-Lymphocytes

Keywords

  • Apoptosis
  • CD95/APO-1
  • Death receptor
  • Thyroid autoimmunity

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Stassi, G., Zeuner, A., Di Liberto, D., Todaro, M., Ricci-Vitiani, L., & De Maria, R. (2001). Fas-FasL in Hashimoto's thyroiditis. Journal of Clinical Immunology, 21(1), 19-23. https://doi.org/10.1023/A:1006732713634

Fas-FasL in Hashimoto's thyroiditis. / Stassi, G.; Zeuner, A.; Di Liberto, D.; Todaro, M.; Ricci-Vitiani, L.; De Maria, R.

In: Journal of Clinical Immunology, Vol. 21, No. 1, 2001, p. 19-23.

Research output: Contribution to journalArticle

Stassi, G, Zeuner, A, Di Liberto, D, Todaro, M, Ricci-Vitiani, L & De Maria, R 2001, 'Fas-FasL in Hashimoto's thyroiditis', Journal of Clinical Immunology, vol. 21, no. 1, pp. 19-23. https://doi.org/10.1023/A:1006732713634
Stassi G, Zeuner A, Di Liberto D, Todaro M, Ricci-Vitiani L, De Maria R. Fas-FasL in Hashimoto's thyroiditis. Journal of Clinical Immunology. 2001;21(1):19-23. https://doi.org/10.1023/A:1006732713634
Stassi, G. ; Zeuner, A. ; Di Liberto, D. ; Todaro, M. ; Ricci-Vitiani, L. ; De Maria, R. / Fas-FasL in Hashimoto's thyroiditis. In: Journal of Clinical Immunology. 2001 ; Vol. 21, No. 1. pp. 19-23.
@article{77ebac5d262a4674b619397093499a2d,
title = "Fas-FasL in Hashimoto's thyroiditis",
abstract = "Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.",
keywords = "Apoptosis, CD95/APO-1, Death receptor, Thyroid autoimmunity",
author = "G. Stassi and A. Zeuner and {Di Liberto}, D. and M. Todaro and L. Ricci-Vitiani and {De Maria}, R.",
year = "2001",
doi = "10.1023/A:1006732713634",
language = "English",
volume = "21",
pages = "19--23",
journal = "Journal of Clinical Immunology",
issn = "0271-9142",
publisher = "Springer New York",
number = "1",

}

TY - JOUR

T1 - Fas-FasL in Hashimoto's thyroiditis

AU - Stassi, G.

AU - Zeuner, A.

AU - Di Liberto, D.

AU - Todaro, M.

AU - Ricci-Vitiani, L.

AU - De Maria, R.

PY - 2001

Y1 - 2001

N2 - Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.

AB - Hashimoto's thyroiditis is a common chronic autoimmune disease characterized by the loss of thyroid follicular cells (thyrocytes) that are gradually replaced by lymphocytic infiltration and diffuse fibrosis. These morphological findings suggested that autoreactive T-cell clones were responsible for thyrocyte destruction and hypothyroidism through effector-target cytotoxic recognition. Later, autonomous interaction between thyrocyte Fas and FasL has been proposed as a major mechanism of thyrocyte depletion in Hashimoto's thyroiditis. Here, we analyze the possible role of Fas and FasL in the pathogenesis of Hashimoto's thyroiditis. We suggest that the Fas-FasL system dictates the outcome of the autoimmune response by acting on both immune and target cells.

KW - Apoptosis

KW - CD95/APO-1

KW - Death receptor

KW - Thyroid autoimmunity

UR - http://www.scopus.com/inward/record.url?scp=0035069523&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035069523&partnerID=8YFLogxK

U2 - 10.1023/A:1006732713634

DO - 10.1023/A:1006732713634

M3 - Article

C2 - 11321234

AN - SCOPUS:0035069523

VL - 21

SP - 19

EP - 23

JO - Journal of Clinical Immunology

JF - Journal of Clinical Immunology

SN - 0271-9142

IS - 1

ER -