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Published online on May 12, 2004, 10.1073/pnas.0402065101
PNAS | May 25, 2004 | vol. 101 | no. 21 | 8102-8107


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IMMUNOLOGY
Natural killer cells distinguish innocuous and destructive forms of pancreatic islet autoimmunity

Laurent Poirot *, Christophe Benoist {dagger}, and Diane Mathis {dagger}

Section on Immunology and Immunogenetics, Joslin Diabetes Center, and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, One Joslin Place, Boston, MA 02215

Contributed by Diane Mathis, March 24, 2004

In both human patients and murine models, the progression from insulitis to diabetes is neither immediate nor inevitable, as illustrated by the innocuous versus destructive infiltrates of BDC2.5 transgenic mice on the nonobese diabetic (NOD) versus C57BL/6.H-2g7 genetic backgrounds. Natural killer (NK)-cell-specific transcripts and the proportion of NK cells were increased in leukocytes from the aggressive BDC2.5/B6.H-2g7 lesions. NK cell participation was also enhanced in the aggressive lesions provoked by CTLA-4 blockade in BDC2.5/NOD mice. In this context, depletion of NK cells significantly inhibited diabetes development. NOD and B6.H-2g7 mice exhibit extensive variation in NK receptor expression, reminiscent of analogous human molecules. NK cells can be important players in type 1 diabetes, a role that was previously underappreciated.

type 1 diabetes | mouse model | microarray

Abbreviations: NK, natural killer; NKC, NK gene complex; NKR, NK receptor; NOD, nonobese diabetic; TCR, T cell receptor.

* Present address: Genomics Institute, Novartis Research Foundation, 10675 John Jay Hopkins Drive, San Diego, CA 92121.

{dagger} To whom correspondence may be addressed. E-mail: cbdm{at}joslin.harvard.edu or dm{at}joslin.harvard.edu.


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