Abstract:
:The presentation of islet antigens in the pancreatic LNs (PLNs) of mice is a developmentally regulated process. It has been hypothesized that, during physiological tissue remodeling, a wave of neonatal β-cell apoptosis may initiate diabetes in autoimmune-prone strains of mice. If true, increasing or decreasing physiological β-cell apoptosis in neonatal NOD mice should alter the time-course of antigen presentation in the PLNs. We used transgenic over-expression of either an anti-apoptotic protein (Bcl-2) or a toxic transgene (rat insulin promoter-Kb) in mouse β cells to reduce or increase neonatal β-cell apoptosis, respectively. Neither intervention affected the timing of antigen presentation in the PLNs or the initiation of islet infiltration. This suggests that under physiological conditions and in the absence of inflammation, neonatal β-cell apoptosis in NOD mice is not the trigger for antigen presentation in the draining LNs.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Carrington EM,Kos C,Zhan Y,Krishnamurthy B,Allison Jdoi
10.1002/eji.201141476subject
Has Abstractpub_date
2011-08-01 00:00:00pages
2238-47issue
8eissn
0014-2980issn
1521-4141journal_volume
41pub_type
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