Abstract:
:Insulitis develops in non-obese diabetic (NOD) mice as a multicentric and asynchronous process. In an effort to understand how this T cell mediated process expands within each islet and propagates between the islets of the same pancreas, we have analyzed the junctional diversity of TCR V beta 6 and V beta 8.2 transcripts cloned from infiltrated islets. The material examined was obtained from individual islets of 8 and 12 week old NOD mice or from pooled islets of 4 week old individual mice. Compared with spleen transcripts, where every V beta 6 or V beta 8.2 clone displays a different junction, islet transcripts are considerably less diverse. Each islet harbors from one to a maximum of six independent CDR3 sequences out of 10 or more analyzed colonies. On the other hand, there is an overall diversity of sequences when comparing the islets of the same pancreas or individual mice at 4 weeks. Altogether, these results support the idea that TCR repertoires are already divergent at the very early onset of insulitis and that each islet-centered infiltrate develops rather autonomously from the oligoclonal expansion of a limited set of precursors. Recirculation between islets is limited and does not seem to be the main mode of propagation of insulitis. Finally, a close analysis of J beta usage and N additions in beta chain transcripts from infiltrating cells reveals definite biases suggestive of an ongoing selective process imposed upon intra-pancreatic T lymphocytes.
journal_name
Int Immunoljournal_title
International immunologyauthors
Sarukhan A,Bedossa P,Garchon HJ,Bach JF,Carnaud Cdoi
10.1093/intimm/7.1.139subject
Has Abstractpub_date
1995-01-01 00:00:00pages
139-46issue
1eissn
0953-8178issn
1460-2377journal_volume
7pub_type
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