Activation of natural killer T cells by α-galactosylceramide treatment prevents the onset and recurrence of autoimmune type 1 diabetes

Nature Medicine

Volumn 7, Issue 9, 2001, Pages 1057-1062

  Sharif, Shayan ^a   Arreaza, Guillermo A ^a   Zucker, Peter ^a   Mi, Qing Sheng ^a   Sondhi, Jitin ^a   Naidenko, Olga V ^b   Kronenberg, Mitchell ^b   Koezuka, Yasuhiko ^c   Delovitch, Terry L ^a,d   Gombert, Jean Marc ^e,f   Leite de Moraes, Maria ^g   Gouarin, Christine ^e   Zhu, Ren ^e   Hameg, Agathe ^e   Nakayama, Toshinori ^h   Taniguchi, Masaru ^h   Lepault, Françoise ^g   Lehuen, Agnès ^e   Bach, Jean François ^e   Herbelin, André ^e  

^a ROBARTS RESEARCH INSTITUTE   (Canada)

^b LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGY   (United States)

^c KIRIN BREWERY CO LTD   (Japan)

^d UNIVERSITY OF WESTERN ONTARIO   (Canada)

^e BICHAT HOSPITAL   (France)

^f POITIERS UNIVERSITY HOSPITAL   (France)

^g HÔPITAL NECKER ENFANTS MALADES   (France)

^h CHIBA UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA GALACTOSYLCERAMIDE; CERAMIDE DERIVATIVE; GLYCOLIPID; INTERLEUKIN 10; INTERLEUKIN 4; INTERLEUKIN 7; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; AUTOIMMUNE DISEASE; AUTOIMMUNITY; B LYMPHOCYTE; CELL ACTIVATION; CELL POLARITY; CELL TRANSPLANTATION; CONTROLLED STUDY; CYTOKINE RELEASE; DISEASE ASSOCIATION; IMMUNOREGULATION; INSULIN DEPENDENT DIABETES MELLITUS; INSULITIS; NATURAL KILLER CELL; NONHUMAN; OBESITY; PANCREAS ISLET CELL; PRIORITY JOURNAL; RECURRENT DISEASE; RISK FACTOR; SURVIVAL; T LYMPHOCYTE; TH1 CELL; TREATMENT PLANNING;

ANIMALS; ANTIBODIES, MONOCLONAL; ANTIGENS, CD1; CYCLOPHOSPHAMIDE; DIABETES MELLITUS, TYPE 1; GALACTOSYLCERAMIDES; INTERFERON TYPE II; INTERLEUKIN-4; INTERLEUKIN-7; KILLER CELLS, NATURAL; L-SELECTIN; LYMPHOCYTE ACTIVATION; MICE; MICE, INBRED BALB C; MICE, INBRED NOD; MICE, MUTANT STRAINS; RECEPTORS, INTERLEUKIN; RECEPTORS, INTERLEUKIN-10; SPLEEN;

EID: 0034799397     PISSN: 10788956     EISSN: None     Source Type: Journal    
DOI: 10.1038/nm0901-1057     Document Type: Article

References (33)

1. The nonobese diabetic mouse as a model of autoimmune diabetes: Immune dysregulation gets the NOD
2. CD1-reactive natural killer T cells are required for development of systemic tolerance through an immune-privileged site
3. NKT cells: Facts, functions and fallacies
4. CD4pos, NK1.1pos T cells promptly produce interleukin 4 in response to in vivo challenge with anti-CD3
5. NK T cell-derived IL-10 is essential for the differentiation of antigen-specific T regulatory cells in systemic tolerance
6. − T-cell deficiency and IDDM in NOD/Lt mice
7. +-like thymocytes in the NOD mouse
8. Extreme Th1 bias of invariant Vα24JαQ T cells in type 1 diabetes
9. Overexpression of natural killer T cells protects Vα14-Jα281 transgenic nonobese diabetic mice against diabetes
10. CD1d-restricted and TCR-mediated activation of Vα14 NKT cells by glycosylceramides
11. Immunization with α-galactosylceramide polarizes CD1-reactive NK T cells towards Th2 cytokine synthesis
12. Activation of NK T cells by CD1d and α-galactosylceramide directs conventional T cells to the acquisition of a Th2 phenotype
13. − (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10
14. Mouse CD1-specific NK1T cells: Development, specificity, and function
15. Regulatory T cells in autoimmunity
16. CD1d-mediated recognition of an α-galactosylceramide by natural killer T cells is highly conserved through mammalian evolution
17. A subset of NKT cells that lacks the NK1.1 marker, expresses CD1d molecules, and autopresents the α-galactosylceramide antigen
18. + T cell-defective IL-4 production in the nonobese diabetic mice
19. + T cells from IL-7-deficient mice have a normal distribution and selection but exhibit impaired cytokine production
20. Anti-suppressor effect of cyclophosphamide on the development of spontaneous diabetes in NOD mice
21. CD4(+) Vα14 natural killer T cells are essential for acceptance of rat islet xenografts in mice
22. Requirement for natural killer T (NKT) cells in the induction of allograft tolerance
23. +TCR α β + (NKT) cells in the nonrecurrent spontaneous diabetic BB rats transplanted with pancreatic duodenal grafts of Wistar-Furth donors
24. Combination therapy with cyclosporine and interleukin-4 or interleukin-10 prolongs survival of synergeneic pancreatic islet grafts in nonobese diabetic mice: Islet graft survival does notcorrelate with mRNA levels of type 1 or type 2 cytokines, or transforming growth factor-beta in the islet grafts
25. Tracking the response of natural killer T cells to a glycolipid antigen using CD1d tetramers
26. Lack of L-selectin expression by cells transferring diabetes in NOD mice: Insights into the mechanisms involved in diabetes prevention by Mel-14 antibody treatment
27. + immunoregulatory T cells that control autoimmune diabetes
28. + thymocytes expressing L-selectin mediate "active tolerance" in the nonobese diabetic mouse
29. + T cells that prevent diabetes onset in nonobese diabetic mice
30. The natural killer T-cell ligand α-galactosylceramide prevents autoimmune diabetes in non-obese diabetic mice
31. Activation of hepatic NKT cells and subsequent liver injury following administration of α-galactosylceramide
32. − T cells
33. NKT cell-induced protection against diabetes in Vα14-Jα281 transgenic NOD mice is associated with a Th2 shift circumscribed regionally to the islets and functionally to islet auto-antigen