Nature Immunology2, 1117 - 1125 (2001)
Published online: 19 November 2001; | doi:10.1038/ni738
Damage control, rather than unresponsiveness, effected by protective DX5+ T cells in autoimmune diabetes
Antonio Gonzalez1, 2, Isabelle Andre-Schmutz1, 3, Claude Carnaud1, 4, Diane Mathis1, 5
& Christophe Benoist1, 5
1
Institut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS/INSERM/ULP), Strasbourg, France.
2
INSERM U25, Hopital Necker, Paris, France.
3
Present address: Laboratorio de Investigación 2, Hospital Clínico Universitario, 15706-Santiago de Compostela, Spain.
4
Present address: INSERM U429, Hopital Necker, 75015, Paris, France.
5
Present address: Section on Immunology and Immunogenetics, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Correspondence should be addressed to Diane MathisChristophe Benoist and D Mathis cbdm@joslin.harvard.edu
The progression of autoimmune diabetes is regulated. We examined here the cellular controls exerted on disease that developed in the BDC2.5 T cell receptor−transgenic model. We found that all BDC2.5 mice with a monoclonal, cell−reactive, T cell repertoire developed diabetes before 4 weeks of age; transfer of splenocytes from young standard NOD (nonobese diabetic) mice into perinatal monoclonal BDC2.5 animals protected them from diabetes. The protective activity was generated by CD4+ T cells, which operated for a short time at disease initiation, could be partitioned according to DX5 cell surface marker expression and split into two components. Protection did not involve clonal deletion or anergy of the autoreactive BDC2.5 cells, permitting their full activation and attack of pancreatic islets; rather, it tempered the aggressiveness of the insulitic lesion and the extent of cell destruction.
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cell−reactive, T cell repertoire developed diabetes before 4 weeks of age; transfer of splenocytes from young standard NOD (nonobese diabetic) mice into perinatal monoclonal BDC2.5 animals protected them from diabetes. The protective activity was generated by CD4+ 
T cells
