Prostaglandin I2 signaling licenses Treg suppressive function and prevents pathogenic reprogramming
نویسندگان
چکیده
منابع مشابه
Multiple treg suppressive modules and their adaptability
Foxp3(+) regulatory T cells (Tregs) are a constitutively immunosuppressive cell type critical for the control of autoimmunity and inflammatory pathology. A range of mechanisms of Treg suppression have been identified and it has not always been clear how these different mechanisms interact in order to properly suppress autoimmunity and excessive inflammation. In recent years it has become clear ...
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Background Enhanced eosinophil extravasation into the tissue is a characteristic feature of bronchial asthma and other allergic diseases. The barrier-forming vascular endothelial cells release prostaglandin I2 (PGI2, prostacyclin) as the major prostanoid, and it has been previously observed that PGI2 receptor (IP)-deficient mice show enhanced eosinophilic inflammation in response to allergens. ...
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BACKGROUND Prostaglandin I(2) (PGI(2)), a lipid mediator currently used in treatment of human disease, is a critical regulator of adaptive immune responses. Although PGI(2) signaling suppressed Th1 and Th2 immune responses, the role of PGI(2) in Th17 differentiation is not known. METHODOLOGY/PRINCIPAL FINDINGS In mouse CD4(+)CD62L(+) naïve T cell culture, the PGI(2) analogs iloprost and cicap...
متن کاملProstaglandin I2-IP signaling promotes Th1 differentiation in a mouse model of contact hypersensitivity.
PGI(2), which exerts its actions via its specific Gs-coupled I prostanoid receptor (IP), is known to be present in the lymph nodes, but its roles in acquired cutaneous immune responses remain unclear. To investigate the role of PGI(2)-IP signaling in cutaneous immune responses, we applied IP-deficient (Ptgir(-/-)) mice to contact hypersensitivity as a model of acquired immune response and found...
متن کاملSignaling through the prostaglandin I2 receptor IP protects against respiratory syncytial virus-induced illness.
The role of prostanoids in modulating respiratory syncytial virus (RSV) infection is unknown. We found that RSV infection in mice increases production of prostaglandin I(2) (PGI(2)). Mice that overexpress PGI(2) synthase selectively in bronchial epithelium are protected against RSV-induced weight loss and have decreased peak viral replication and gamma interferon levels in the lung compared to ...
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ژورنال
عنوان ژورنال: Journal of Clinical Investigation
سال: 2021
ISSN: 0021-9738,1558-8238
DOI: 10.1172/jci140690