Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 198, Issue 10, Pages 1527-1537Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20030966
Keywords
autoimmune response; pancreas; PLN; antigen transport; apoptosis
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Funding
- NIDDK NIH HHS [P30 DK036836, P30DK36836-16, R01 DK059658, R01DK59658-02] Funding Source: Medline
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The prelude to type-1 diabetes is leukocyte infiltration into the pancreatic islets, or insulitis. This process begins in pancreatic lymph nodes when T lymphocytes reactive to islet beta cells encounter antigen-presenting cells (APCs) displaying peptides derived from beta cell proteins. We show here that a ripple of physiological beta cell death, which occurs at 2 wk of age in all mouse strains, precipitates the arrival of such APCs, and that the relevant APC is a dendritic cell of CD11c(+)CD11b(+)CD8alpha(-) phenotype. These findings have significant implications concerning the nature of the diabetes-provoking deficits in NOD mice, the identity of the primordial diabetogenic antigens, and our understanding of the balance between immunity and tolerance in a pathological context.
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