Diagnostic significance of serum concentrations of soluble Fas ligand (sFasL) in children with autoimmune thyroid disease

Autoimmunity ◽  
2017 ◽  
Vol 50 (3) ◽  
pp. 192-198 ◽  
Author(s):  
Hanna Mikos ◽  
Marcin Mikos ◽  
Marek Niedziela
Thyroid ◽  
2004 ◽  
Vol 14 (10) ◽  
pp. 819-824 ◽  
Author(s):  
Yukiyo Nakamura ◽  
Mikio Watanabe ◽  
Fumio Matsuzuka ◽  
Hayato Maruoka ◽  
Akira Miyauchi ◽  
...  

2000 ◽  
Vol 263 (3) ◽  
pp. 108-110 ◽  
Author(s):  
H. Iwama ◽  
H. Akutsu ◽  
S. Kuretake ◽  
J. Tohma ◽  
N. Nakamura

2003 ◽  
pp. 393-396 ◽  
Author(s):  
BJ Stuck ◽  
MA Pani ◽  
F Besrour ◽  
M Segni ◽  
M Krause ◽  
...  

BACKGROUND: Apoptosis is a joint pathogenic process underlying autoimmune thyroid disease. Increased programmed cell death in thyrocytes causes hypothyroidism in Hashimoto's thyroiditis, whereas in Graves' disease infiltrating lymphocytes undergo apoptosis while thyrocytes appear to proliferate under protection of anti-apoptotic signals. The Fas/Fas ligand cascade represents a major pathway initiating apoptosis. Its role in autoimmunity is well studied and genetic polymorphisms in gene loci of Fas and its ligand have been shown to be associated with autoimmune diseases. OBJECTIVE: Due to the functional relevance of the Fas pathway in autoimmune thyroid disease we were interested in the possible contribution of polymorphisms in the Fas gene to the genetic risk of thyroid autoimmunity, which so far is mainly, but incompletely, attributed to the HLA DQ region and polymorphisms in the CTLA-4 gene. DESIGN: We genotyped Caucasian families with at least one offspring affected by Hashimoto's thyroiditis (n=95) and Graves' disease (n=109) for two Fas gene polymorphisms (g-670 G-->A in the promoter region, g-154 C-->T in exon 7). METHODS: Extended transmission disequilibrium and chi(2) testing were performed. RESULTS: Neither polymorphism alone (P=0.44 and P=0.70) nor the promoter/exon 7 haplotypes (P=0.86) were associated with Hashimoto's thyroiditis. No association with Graves' disease was observed for the promoter polymorphism (P=0.91) and exon 7 (P=0.65) or the promoter/exon 7 haplotypes (P=0.80). CONCLUSION: In summary, our data do not suggest any significant contribution of common genetic Fas variants to the genetic risk of developing Hashimoto's thyroiditis or Graves' disease.


2004 ◽  
Vol 73 (2) ◽  
pp. 244-249 ◽  
Author(s):  
Le H. Song ◽  
Vu Q. Binh ◽  
Dinh N. Duy ◽  
Thomas C. Bock ◽  
Peter G. Kremsner ◽  
...  

Thyroid ◽  
2004 ◽  
Vol 14 (10) ◽  
pp. 819-824 ◽  
Author(s):  
Yukiyo Nakamura ◽  
Mikio Watanabe ◽  
Fumio Matsuzuka ◽  
Hayato Maruoka ◽  
Akira Miyauchi ◽  
...  

Pteridines ◽  
2000 ◽  
Vol 11 (3) ◽  
pp. 85-89
Author(s):  
Barbara Wirleitner ◽  
Elisabeth Kowald ◽  
Bernhard Widner ◽  
Ulrike Ortner ◽  
Gabriele Baier-Bitterlich ◽  
...  

SummaryEvidence accumulates suggesting that the pathogenesis in systemic lupus erythematosus (SLE) is associated with modulations in the Fas/FasL system. Serum concentrations of soluble Fas ligand (sFasL) were found to be elevated in patients with SLE. In this study we wanted to determine the levels of sFasL and the status of immune activation - monitored by neopterin secretion - in patients with SLE and cutaneous discoid lupus erythematosus (CDLE). Sixty-five serum samples were assayed. We found elevated concentrations of sFasL in patients with SLE and CDLE. The levels of sFasL in COLE patients were significant lower compared to SLE patients. Neopterin concentrations in serum were found to be slightly increased in patients with CDLE. Compared to patients with SLE, activation of the immune system was significant lower in COLE. Taken together, we found d evated levels of sFasL in patients with SLE as well as CDLE, connected with ar activation of the immune system and thereby increased concentration of neopterin in serum.


Praxis ◽  
2002 ◽  
Vol 91 (27) ◽  
pp. 1151-1160
Author(s):  
Fajfr ◽  
Müller

Les maladies thyroïdiennes auto-immunes ou immunes (autoimmune thyroid disease, AITD) sont relativement fréquentes. Le terme de AITD comprend les thyréodites euthyroidiennes ou hypothyroïdiennes de Hashimoto avec ou sans goitre, les hyperthyroïdies classiques de Basedow et leurs variantes nettement plus rares euthyroïdiennes ou hypothyroïdiennes. Aucune des nombreuses classifications des AITD n'a pu s'imposer sur le plan international. La pathogénèse de toutes les formes d'AITD comprend une perturbation de la tolérance immune chez les individus prédisposés génétiquement (séquence HLA-DQAI*0501 sur le bras court du chromosome 6) qui provoque un processus auto-immun contre la glande thyroïdienne. Ces processus sont soit destructeurs ou inhibiteurs, soit stimulateurs, ce qui permet d'expliquer les formes très différentes de AITD. Dans de cas rares, ces processus peuvent se contrebalancer («balance hypotheseis»). Les anticorps anti-récepteurs TPO et TSH (TRAK) ont une place particulière dans le diagnostic des AITD. Les dosages de routine utilisent pour la mesure des TRAK des récepteurs qui ne peuvent pas différencier entre les anticorps stimulants ou bloquants contre les récepteurs TSH. C'est, entre autre pour ces raisons, que les résultats d'anticorps positifs ne sont utilisables qu'en connaissance de la clinique et / ou des paramètres de la fonction thyroïdienne. Ce travail présente quatre patients avec des formes plus complexes d'AITD et résume les connaissances actuelles.


Pneumologie ◽  
2012 ◽  
Vol 66 (11) ◽  
Author(s):  
C Ravaglia ◽  
C Gurioli ◽  
M Romagnoli ◽  
G Casoni ◽  
S Tomassetti ◽  
...  

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