Abstract:
: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.
journal_name
Proc Natl Acad Sci U S Aauthors
Poirot L,Benoist C,Mathis Ddoi
10.1073/pnas.0402065101keywords:
subject
Has Abstractpub_date
2004-05-25 00:00:00pages
8102-7issue
21eissn
0027-8424issn
1091-6490pii
0402065101journal_volume
101pub_type
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