In:
The Journal of Immunology, The American Association of Immunologists, Vol. 200, No. 1_Supplement ( 2018-05-01), p. 47.18-47.18
Abstract:
Our laboratory has shown in recent years that prostaglandin I2 (PGI2) promotes immune tolerance through inhibition of T cell and dendritic cell function. Specifically, we have shown that PGI2 is able to restrain Th1 and Th2 immune responses, suggesting that it has immunosuppressive properties. However, PGI2’s impact on the functionality of T regulatory (Treg) cells, a T cell subtype important for the suppression/resolution of immune responses which express the canonical transcription factor forkhead box p3 (Foxp3), is unknown. Thus, we hypothesized that PGI2 promotes the function of Tregs. To test this hypothesis, we utilized mice deficient in IP (IP KO), the receptor for PGI2.. We found that splenic Tregs from IP KO mice have a significantly lower mean fluorescence intensity (MFI) of Foxp3 compared to wild-type (WT) Tregs. Furthermore, the percent suppression of CFSE-stained WT effector T cells by IP KO Tregs was significantly decreased compared to the percent suppression of CFSE-stained WT effector T cells by WT Tregs. Moreover, the percentage of induced Tregs (iTregs) generated from naïve T cells isolated from IP KO mice was significantly reduced compared to WT mice. As a whole, our preliminary data demonstrate the ability of PGI2 to promote Treg function, and thus suggest that PGI2 may serve as a novel treatment strategy for T cell mediated diseases.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.200.Supp.47.18
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2018
detail.hit.zdb_id:
1475085-5
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