Proinflammatory cytokines contribute to development and function of regulatory T cells in type 1 diabetes

Thomas, Helen E., Graham, Kate L., Chee, Jonathan, Thomas, Ranjeny, Kay, Thomas W. and Krishnamurthy, Balasubramanian (2013). Proinflammatory cytokines contribute to development and function of regulatory T cells in type 1 diabetes. In: Narinder K. Mehra, Translational immunology in Asia-Oceania. 5th FIMSA Congress, New Dehli, India, (81-86). 14 -17 March 2012. doi:10.1111/j.1749-6632.2012.06797.x


Author Thomas, Helen E.
Graham, Kate L.
Chee, Jonathan
Thomas, Ranjeny
Kay, Thomas W.
Krishnamurthy, Balasubramanian
Title of paper Proinflammatory cytokines contribute to development and function of regulatory T cells in type 1 diabetes
Conference name 5th FIMSA Congress
Conference location New Dehli, India
Conference dates 14 -17 March 2012
Proceedings title Translational immunology in Asia-Oceania   Check publisher's open access policy
Journal name Annals of the New York Academy of Sciences   Check publisher's open access policy
Place of Publication Hoboken, NJ 07030 United States
Publisher Wiley-Blackwell Publishing, Inc.
Publication Year 2013
Year available 2012
Sub-type Fully published paper
DOI 10.1111/j.1749-6632.2012.06797.x
Open Access Status Not yet assessed
ISBN 9781573318662
ISSN 0077-8923
1749-6632
Editor Narinder K. Mehra
Volume 1283
Start page 81
End page 86
Total pages 6
Language eng
Abstract/Summary Type 1 diabetes is caused by immune-mediated loss of pancreatic beta cells. It has been proposed that inflammatory cytokines play a role in killing beta cells. Expression of interleukin (IL)-1 and tumor necrosis factor (TNF-alpha) has been detected in islets from patients with type 1 diabetes, and these cytokines can induce beta cell death in vitro. We produced nonobese diabetic (NOD) mice lacking receptors for these cytokines. Islets from mice lacking IL-1RI or TNFR1 were killed when transplanted into wild-type NOD mice, suggesting that cytokine action on beta cells is not required for killing. Mice lacking TNFR1 did not develop diabetes, and mice lacking IL-1R had delayed onset of diabetes, indicating a role for these cytokines in disease development. TNFR1-deficient mice had an increased number of CD4(+)CD25(+)FoxP3(+) regulatory T cells with enhanced suppressive capacity. IL-1 was produced at higher levels in NOD mice and resulted in dilution of suppressor function of CD4(+)CD25(+)FoxP3(+) regulatory T cells. Our data suggest that blocking inflammatory cytokines may increase the capacity of the immune system to suppress type 1 diabetes through regulatory T cells.
Keyword Diabetes
Regulatory T cells
Nod Mice
Islet Antigens
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID APP516700
APP502605
Institutional Status UQ

Document type: Conference Paper
Sub-type: Translational Immunology in Asia-Oceania
Collections: Official 2014 Collection
UQ Diamantina Institute Publications
 
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