The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism

المؤلفون المشاركون

Baron, Byron
Farrugia, Mark

المصدر

International Journal of Inflammation

العدد

المجلد 2017، العدد 2017 (31 ديسمبر/كانون الأول 2017)، ص ص. 1-12، 12ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2017-05-03

دولة النشر

مصر

عدد الصفحات

12

التخصصات الرئيسية

الأمراض
الطب البشري

الملخص EN

Toll-like receptors (TLRs), part of the innate immune system that recognises molecular signatures, are important in the recognition of pathogenic components.

However, when specific cellular contexts develop in which TLRs are inappropriately activated by self-components, this may lead to sterile inflammation and result in the occurrence of autoimmunity.

This review analyses the available data regarding TLR biochemistry, the specific mechanisms which are brought about by TLR activation, and the importance of these mechanisms in the light of any existing and potential therapies in the field of autoimmunity.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Farrugia, Mark& Baron, Byron. 2017. The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism. International Journal of Inflammation،Vol. 2017, no. 2017, pp.1-12.
https://search.emarefa.net/detail/BIM-1167492

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Farrugia, Mark& Baron, Byron. The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism. International Journal of Inflammation No. 2017 (2017), pp.1-12.
https://search.emarefa.net/detail/BIM-1167492

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Farrugia, Mark& Baron, Byron. The Role of Toll-Like Receptors in Autoimmune Diseases through Failure of the Self-Recognition Mechanism. International Journal of Inflammation. 2017. Vol. 2017, no. 2017, pp.1-12.
https://search.emarefa.net/detail/BIM-1167492

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1167492