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Cited by 347

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Physiological β Cell Death Triggers Priming of Self-reactive T Cells by Dendritic Cells in a Type-1 Diabetes Model

Open access
Turley, Shannon, Poirot, Laurent, Hattori, Masakazu, Benoist, Christophe, Mathis, Diane·2003·The Journal of Experimental Medicine

Abstract

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 β cells encounter antigen-presenting cells (APCs) displaying peptides derived from β cell proteins. We show here that a ripple of physiological β 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+CD8α− 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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Crossref · 10.1084/jem.20030966

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Metadata

Authors
Turley, S., Poirot, L., Hattori, M., Benoist, C., & Mathis, D.
Venue
The Journal of Experimental Medicine
Published
2003-11-17
Volume
198
Issue
10
Pages
1527-1537
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2127788605
Cited by
347
References
1
FWCI
10.72
Type
journal article
Language
en
Open access
green

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Turley, S., Poirot, L., Hattori, M., Benoist, C., & Mathis, D. (2003). Physiological β Cell Death Triggers Priming of Self-reactive T Cells by Dendritic Cells in a Type-1 Diabetes Model. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20030966

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