A TLR9 agonist promotes IL-22-dependent pancreatic islet allograft survival in type 1 diabetic mice

Deepak Tripathi, Sambasivan Venkatasubramanian, Satyanarayana S. Cheekatla, Padmaja Paidipally, Elwyn Welch, Amy R. Tvinnereim and Ramakrishna Vankayalapati ()
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Deepak Tripathi: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Sambasivan Venkatasubramanian: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Satyanarayana S. Cheekatla: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Padmaja Paidipally: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Elwyn Welch: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Amy R. Tvinnereim: Center for Biomedical Research, University of Texas Health Science Center at Tyler
Ramakrishna Vankayalapati: Center for Biomedical Research, University of Texas Health Science Center at Tyler

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Pancreatic islet transplantation is a promising potential cure for type 1 diabetes (T1D). Islet allografts can survive long term in the liver parenchyma. Here we show that liver NK1.1+ cells induce allograft tolerance in a T1D mouse model. The tolerogenic effects of NK1.1+ cells are mediated through IL-22 production, which enhances allograft survival and increases insulin secretion. Increased expression of NKG2A by liver NK1.1+ cells in islet allograft-transplanted mice is involved in the production of IL-22 and in the reduced inflammatory response to allografts. Vaccination of T1D mice with a CpG oligonucleotide TLR9 agonist (ODN 1585) enhances expansion of IL-22-producing CD3-NK1.1+ cells in the liver and prolongs allograft survival. Our study identifies a role for liver NK1.1+ cells, IL-22 and CpG oligonucleotides in the induction of tolerance to islet allografts in the liver parenchyma.

Date: 2016
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DOI: 10.1038/ncomms13896

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