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CD4(+) type II NKT cells mediate ICOS and programmed death-1-dependent regulation of type 1 diabetes.

Journal article
Authors Nadir Kadri
Eva Korpos
Shashank Gupta
Claire Briet
Linda Löfbom
Hideo Yagita
Agnes Lehuen
Christian Boitard
Dan Holmberg
Lydia Sorokin
Susanna Cardell
Published in Journal of immunology
Volume 188
Issue 7
Pages 3138-49
ISSN 1550-6606
Publication year 2012
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Pages 3138-49
Language en
Links dx.doi.org/10.4049/jimmunol.1101390
Keywords Adoptive Transfer, Animals, Antigens, CD1d, immunology, Antigens, CD274, physiology, Apoptosis, immunology, CD4-Positive T-Lymphocytes, classification, immunology, transplantation, Diabetes Mellitus, Type 1, immunology, prevention & control, Disease Models, Animal, Immunologic Memory, Inducible T-Cell Co-Stimulator Protein, physiology, Lymph Nodes, immunology, Mice, Mice, Inbred NOD, Mice, SCID, Mice, Transgenic, Natural Killer T-Cells, classification, immunology, transplantation, Pancreas, immunology, Pancreatitis, prevention & control, Receptors, Antigen, T-Cell, genetics, immunology, Specific Pathogen-Free Organisms, T-Lymphocyte Subsets, immunology, transplantation, T-Lymphocytes, Regulatory, immunology
Subject categories Microbiology in the medical area

Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease that results from T cell-mediated destruction of pancreatic β cells. CD1d-restricted NKT lymphocytes have the ability to regulate immunity, including autoimmunity. We previously demonstrated that CD1d-restricted type II NKT cells, which carry diverse TCRs, prevented T1D in the NOD mouse model for the human disease. In this study, we show that CD4(+) 24αβ type II NKT cells, but not CD4/CD8 double-negative NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive transfer experiments. CD4(+) 24αβ NKT cells exhibited a memory phenotype including high ICOS expression, increased cytokine production, and limited display of NK cell markers, compared with double-negative 24αβ NKT cells. Blocking of ICOS or the programmed death-1/programmed death ligand 1 pathway was shown to abolish the regulation that occurred in the pancreas draining lymph nodes. To our knowledge, these results provide for the first time cellular and molecular information on how type II CD1d-restricted NKT cells regulate T1D.

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