PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis

المؤلفون المشاركون

Racke, Michael K.
Lovett-Racke, Amy
Drew, Paul D.
Yang, Yuhong
Gocke, Anne R.

المصدر

PPAR Research

العدد

المجلد 2008، العدد 2008 (31 ديسمبر/كانون الأول 2008)، ص ص. 1-6، 6ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2008-06-26

دولة النشر

مصر

عدد الصفحات

6

التخصصات الرئيسية

الأحياء

الملخص EN

PPARs are members of the steroid hormone nuclear receptor superfamily and play an important role in the regulation of lipid metabolism, energy balance, artherosclerosis and glucose control.

Recent studies suggest that they play an important role in regulating inflammation.

This review will focus on PPAR-α regulation of the immune response.

We describe how PPAR-α regulates differentiation of T cells by transactivation and/or interaction with other transcription factors.

Moreover, PPAR-α agonists have been shown to ameliorate experimental autoimmune encephalomyelitis (EAE) in mice, suggesting that they could provide a therapy for human autoimmune diseases such as multiple sclerosis.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Yang, Yuhong& Gocke, Anne R.& Lovett-Racke, Amy& Drew, Paul D.& Racke, Michael K.. 2008. PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis. PPAR Research،Vol. 2008, no. 2008, pp.1-6.
https://search.emarefa.net/detail/BIM-988217

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Yang, Yuhong…[et al.]. PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis. PPAR Research No. 2008 (2008), pp.1-6.
https://search.emarefa.net/detail/BIM-988217

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Yang, Yuhong& Gocke, Anne R.& Lovett-Racke, Amy& Drew, Paul D.& Racke, Michael K.. PPAR Alpha Regulation of the Immune Response and Autoimmune Encephalomyelitis. PPAR Research. 2008. Vol. 2008, no. 2008, pp.1-6.
https://search.emarefa.net/detail/BIM-988217

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-988217