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Prevention of diabetes in nonobese diabetic mice mediated by CD1d-restricted nonclassical NKT cells

Duarte, N; Stenström, Martin LU ; Campino, S; Bergman, ML; Lundholm, M; Holmberg, D and Cardell, Susanna LU (2004) In Journal of Immunology 173(5). p.3112-3118
Abstract
A role for regulatory lymphocytes has been demonstrated in the pathogenesis of type I diabetes in the NOD mouse but the nature of these cells is debated. CD1d-restricted NKT lymphocytes have been implicated in this process. Previous reports of reduced diabetes incidence in NOD mice in which the numbers of NKT cells are artificially increased have been attributed to the enhanced production of IL-4 by these cells and a role for classical NKT cells, using the Valpha14-Jalpha18 rearrangement. We now show that overexpression in NOD mice of CD1d-restricted TCR Valpha3.2(+)Vbeta9(+) NKT cells producing high levels of IFN-gamma but low amounts of IL-4 leads to prevention of type 1 diabetes, demonstrating a role for nonclassical CD1d-restricted NKT... (More)
A role for regulatory lymphocytes has been demonstrated in the pathogenesis of type I diabetes in the NOD mouse but the nature of these cells is debated. CD1d-restricted NKT lymphocytes have been implicated in this process. Previous reports of reduced diabetes incidence in NOD mice in which the numbers of NKT cells are artificially increased have been attributed to the enhanced production of IL-4 by these cells and a role for classical NKT cells, using the Valpha14-Jalpha18 rearrangement. We now show that overexpression in NOD mice of CD1d-restricted TCR Valpha3.2(+)Vbeta9(+) NKT cells producing high levels of IFN-gamma but low amounts of IL-4 leads to prevention of type 1 diabetes, demonstrating a role for nonclassical CD1d-restricted NKT cells in the regulation of autoimmune diabetes. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Immunology
volume
173
issue
5
pages
3112 - 3118
publisher
American Association of Immunologists
external identifiers
  • wos:000223529800033
  • pmid:15322171
  • scopus:4344605002
ISSN
1550-6606
language
English
LU publication?
yes
id
2a662924-c5f3-49cf-82ae-b8ea40cb7d3d (old id 268498)
alternative location
http://www.jimmunol.org/cgi/content/abstract/173/5/3112
date added to LUP
2007-10-24 11:34:00
date last changed
2017-09-17 07:19:13
@article{2a662924-c5f3-49cf-82ae-b8ea40cb7d3d,
  abstract     = {A role for regulatory lymphocytes has been demonstrated in the pathogenesis of type I diabetes in the NOD mouse but the nature of these cells is debated. CD1d-restricted NKT lymphocytes have been implicated in this process. Previous reports of reduced diabetes incidence in NOD mice in which the numbers of NKT cells are artificially increased have been attributed to the enhanced production of IL-4 by these cells and a role for classical NKT cells, using the Valpha14-Jalpha18 rearrangement. We now show that overexpression in NOD mice of CD1d-restricted TCR Valpha3.2(+)Vbeta9(+) NKT cells producing high levels of IFN-gamma but low amounts of IL-4 leads to prevention of type 1 diabetes, demonstrating a role for nonclassical CD1d-restricted NKT cells in the regulation of autoimmune diabetes.},
  author       = {Duarte, N and Stenström, Martin and Campino, S and Bergman, ML and Lundholm, M and Holmberg, D and Cardell, Susanna},
  issn         = {1550-6606},
  language     = {eng},
  number       = {5},
  pages        = {3112--3118},
  publisher    = {American Association of Immunologists},
  series       = {Journal of Immunology},
  title        = {Prevention of diabetes in nonobese diabetic mice mediated by CD1d-restricted nonclassical NKT cells},
  volume       = {173},
  year         = {2004},
}