Journal
SCIENTIFIC REPORTS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-21477-9
Keywords
-
Categories
Funding
- national institutes of health [AI088201]
- Department of Pulmonary Immunology, University of Texas Health Science Center at Tyler, Tyler
Ask authors/readers for more resources
CD4+CD25+FoxP3+ cells (Tregs) inhibit inflammatory immune responses to allografts. Here, we found that co-transplantation of allogeneic pancreatic islets with Tregs that are defective in c-Jun N-terminal kinase 1 (JNK1) signaling prolongs islet allograft survival in the liver parenchyma of chemically induced diabetic mice (CDM). Adoptively transferred JNK1(-/-) but not wild-type (WT) Tregs survive longer in the liver parenchyma of CDM. JNK1(-/-) Tregs are resistant to apoptosis and express anti-apoptotic molecules. JNK1(-/-) Tregs express higher levels of lymphocyte activation gene-3 molecule (LAG-3) on their surface and produce higher amounts of the anti-inflammatory cytokine interleukin (IL)-10 compared with WT Tregs. JNK1(-/-) Tregs inhibit liver alloimmune responses more efficiently than WT Tregs. JNK1(-/-) but not WT Tregs are able to inhibit IL-17 and IL-21 production through enhanced LAG-3 expression and IL-10 production. Our study identifies a novel role of JNK1 signaling in Tregs that enhances islet allograft survival in the liver parenchyma of CDM.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available