Apoptosis and autoimmune thyroid disease: following a TRAIL to thyroid destruction?

Bretz, James D.; Baker, James R.

doi:10.1046/j.1365-2265.2001.01345.x

Cited by 45 publications

(49 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, not all transformed tumor cells are susceptible to the TRAIL death pathway [40,58]. The major factors that determine the susceptibility remain unclear [37,52]. There might be some unidentified changes not related to transformation leading to the susceptibility to TRAIL-mediated apoptosis in the primary beta cells.…”

Section: Discussionmentioning

confidence: 99%

“…FADD in turn recruits caspase 8 to form the death-inducing signalling complex, which leads to activation of a caspase cascade and eventual cell death. While the activating events start different signal cascades, all of these communications feed into a final, common apoptotic pathway that leads to cell death [36,37]. However, the role of FADD in TRAIL receptors is highly controversial.…”

Section: Multiple Factors Influenced the Susceptibility Of Normal Islmentioning

confidence: 99%

See 1 more Smart Citation

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

Metzger

Wang

et al. 2002

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis. The aim of this study is to investigate whether apoptosis in human beta cells can be related to the induction of the tumor necrosis factorrelated apoptosis-inducing ligand (TRAIL) pathway. Methods. We examined the expression of TRAIL and TRAIL receptors in two human pancreatic beta-cell lines and in human primary islet cells using RT-PCR assays and flow cytometric analyses and tested TRAIL-mediated beta-cell destruction in 51 Cr release cytotoxicity assays, Annexin-V and APO-DIREC assays.Results. Most of the human beta cells express TRAIL receptors-R1, -R2, -R3, -R4 and/or TRAIL. TRAIL induced much stronger cytotoxicity and apoptosis to beta-cell lines CM and HP62 than did FasL, TNF-α, LTα1β2, LTα2β1, LIGHT, and IFN-γ. The cytotoxicity and apoptosis induced by TRAIL to beta-cell lines CM were inhibited competitively by soluble TRAIL receptors, R1, R2, R3 or R4. Treatment of these beta cells with antibodies against TRAIL receptors was able to block the cytotoxicity of TRAIL to these cells. Beta-cell antigen-specific CTL (CD4 + and CD8 + ) clones express TRAIL, suggesting that these cells are potential sources of TRAIL-inducing betacell destruction. Normal primary islet cells from most donors are resistant to the cytotoxicity mediated by TRAIL. However, treatment with an inhibitor of protein synthesis (cycloheximide) or with an enzyme (PI-PLC) that can remove TRAIL-R3 from the isletcell membrane was able to increase the susceptibility of TRAIL-resistant primary islet cells to the TRAIL death pathway. Conclusion/interpretation. The TRAIL death pathway is present and can function in human islet beta cells, but unidentified inhibitors of the TRAIL death pathway are present in normal islet cells. [Diabetologia (2002[Diabetologia ( ) 45:1678[Diabetologia ( -1688

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Multiple Factors Influenced the Susceptibility Of Normal Islmentioning

confidence: 99%

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

Metzger

Wang

et al. 2002

Diabetologia

View full text Add to dashboard Cite

show abstract

“…Proinflammatory cytokines, such as TNF-α and IL1, can affect immunityrelated apoptosis. TNF-α and IL1 in combination with IFN-γ have been shown to induce apoptosis in thyroid cell culture studies [21][22][23] . The mechanism of apoptosis in HT seems to be associated with the stimulation of cytokines secreted from local lymphocytes 23 .…”

Section: Cumhuriyet Medical Journalmentioning

confidence: 99%

The effect of Vitamin D treatment on thyroid function and the levels of thyroid autoantibodies, TNF-α, IL-6, IL-1β in patients with autoimmune thyroiditis

Acibucu

Dökmetaş

Kilicli

et al. 2016

Cumhuriyet Medical Journal

View full text Add to dashboard Cite

SUMMARYObjective: To investigate the relationship between autoimmune thyroid disease and vitamin D treatment. Method: Fifty four (54) patients with both vitamin D deficiency and newly diagnosed euthyroid Hashimoto's thyroiditis (HT) were recruited for this study. The patients were given intramuscular administration of cholecalciferol at a dose of 300,000 IU/month for 3 months. At the time of diagnoses and after the treatment of vitamin D, free T3 (FT3), free T4 (FT4), thyroid stimulating hormone (TSH), antithyroid peroxidase (anti-TPO), antithyroglobulin (anti-TG), 25 (OH) D3, parathormone (PTH), calcium (Ca), phosphorus (P) and alkaline phosphatase (ALP) levels were measured in all patients; TNF-a, IL-6 and IL-1ß levels were measured in only 43 patients. Results: A statistically significant difference (p˂0.05) was observed between the pre and post treatment FT4, TSH, antiTPO, antiTG, PTH and ALP levels. After the treatment of vitamin D, a statistically significant increase was found in 25 (OH) D3 and FT4 levels, and a significant decrease was found in TSH, antiTPO, antiTG, PTH and ALP levels, whereas no significant difference was noted in FT3, Ca, P, TNF-a, IL-6 and IL-1ß levels. Further, levels of vitamin D were not correlated with FT3, FT4, TSH, antiTPO, antiTG, TNF-a, IL-6 and IL-1ß levels (p˃0.05). CMJCumhuriyet Medical Journal stimulan hormon (TSH), anti tiroid peroksidaz (TPO) ve anti tiroglobulin (TG), 25(OH)D3, parathormon (PTH), kalsiyum (Ca), fosfor (P) ve alkalen fosfataz (ALP) seviyeleri ve yalnız 43 hastada TNF-α, IL-6, IL-1b seviyeleri ölçüldü. Bulgular: Tedavi öncesi ve sonrası FT4, TSH, antiTPO, antiTG, PTH ve ALP seviyeleri açısından arada istatistiksel olarak anlamlı fark vardı (p<0.05). D vitamini tedavi sonrasında 25 (OH) D3 ve FT4 seviyelerinde istatiksel olarak önemli bir artış olurken TSH, antiTPO, antiTG, PTH ve ALP seviyelerinde ise önemli bir düşüş gözlendi. FT3, Ca, P, TNF-α, IL-6 ve IL-1b açısından önemli bir fark yoktu. D vitamini seviyesi ile FT3, FT4, TSH, antiTPO, antiTG, TNF-α, IL-6 ve IL-1b arasında bir korelasyon yoktu. Sonuç: D vitamini eksikliği ve yeni tanı HT'i olan hastalarda D vitamini tedavisinin tiroid antijenitesi ve tiroid fonksiyonu üzerine olumlu yönde etkisi vardır.

show abstract

“…Данные популяционных, генетиче-ских и иммуногенетических исследований позволяют считать, что основой аутоиммунных заболеваний ЩЖ в большей степени является биологическая детерми-нанта, чем социальная. То есть основным этиологиче-ским фактором служит наследственность, в то время как средовые факторы играют второстепенную роль, способствуя реализации генотипа и модулируя ауто-иммунный процесс [17]. С точки зрения формальной генетики аутоиммунные заболевания ЩЖ относятся к мультифакториальным заболеваниям.…”

unclassified

Аутоиммунный синдром перекреста (overlap-синдром) при заболеваниях щитовидной железы — Terra incognita тиреоидологии

Hendeleka

2021

Mìžnarodnij endokrinologìčnij žurnal

View full text Add to dashboard Cite

Довольно частой патологией щитовидной железы (ЩЖ) являются аутоиммунные заболевания. Однако наряду с традиционными аутоиммунными заболеваниями ЩЖ — диффузным токсическим зобом, аутоиммунным тиреоидитом — в клинической практике встречаются синдромы аутоиммунного перекреста (overlap-синдромы), которые характеризуются комбинацией клинических, биохимических и серологических проявлений, свойственных нескольким заболеваниям этого органа. Термин «overlap-синдром» (синдром перекреста) означает, что у одного больного наблюдаются признаки двух различных аутоиммунных заболеваний, имеющих, вероятно, общий патогенез. Пока этиология аутоиммунных заболеваний ЩЖ остается известной не до конца, нельзя однозначно решить, является ли overlap-синдром самостоятельным заболеванием или вариантом течения того или иного аутоиммунного заболевания ЩЖ. Изучение синдрома перекреста необходимо для решения важной проблемы тиреоидологии — разработки методов лечения данной категории больных.

show abstract

Apoptosis and autoimmune thyroid disease: following a TRAIL to thyroid destruction?

Cited by 45 publications

References 91 publications

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

The effect of Vitamin D treatment on thyroid function and the levels of thyroid autoantibodies, TNF-α, IL-6, IL-1β in patients with autoimmune thyroiditis

Аутоиммунный синдром перекреста (overlap-синдром) при заболеваниях щитовидной железы — Terra incognita тиреоидологии

Contact Info

Product

Resources

About

Apoptosis and autoimmune thyroid disease: following a TRAIL to thyroid destruction?

Cited by 45 publications

References 91 publications

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

TNF-Related Apoptosis-Inducing Ligand Death Pathway-Mediated Human Beta-Cell Destruction

The effect of Vitamin D treatment on thyroid function and the levels of thyroid autoantibodies, TNF-α, IL-6, IL-1β in patients with autoimmune thyroiditis

Аутоиммунный синдром перекреста (overlap-синдром) при заболеваниях щитовидной железы — ​Terra incognita тиреоидологии

Contact Info

Product

Resources

About

Аутоиммунный синдром перекреста (overlap-синдром) при заболеваниях щитовидной железы — Terra incognita тиреоидологии