Rel B is an early marker of autoimmune islet inflammation in the BioBreeding (BB) rat
Bieg, Sabine ; Simonson, William T ; Ellefsen, Kristian and Lernmark, Åke LU
(2000)
In Pancreas
20(1).
p.47-54
- Abstract
Because the development of insulitis and diabetes is predictable in Lyp/Lyp congenic BB rats, we have characterized early islet inflammation in these rats to determine the cell subsets involved in the onset of autoimmune insulitis. Pancreas sections from prediabetic Lyp/Lyp, Lyp/+ and +/+ rats were analyzed by immunohistochemistry. We found W3/25+ cells in the exo- and endocrine tissue from all three genotypes, but intraislet insulitis was never found in Lyp/+ or +/+ rats. The onset of massive, intraislet B- and T-cell infiltration in Lyp/Lyp rats was preceded by Rel B+ cells in and around the islets, followed by ED1+ monocytes/macrophages. Rel B+ cells were more frequent in the parafollicular cortex of pancreatic lymph nodes from... (More)
Because the development of insulitis and diabetes is predictable in Lyp/Lyp congenic BB rats, we have characterized early islet inflammation in these rats to determine the cell subsets involved in the onset of autoimmune insulitis. Pancreas sections from prediabetic Lyp/Lyp, Lyp/+ and +/+ rats were analyzed by immunohistochemistry. We found W3/25+ cells in the exo- and endocrine tissue from all three genotypes, but intraislet insulitis was never found in Lyp/+ or +/+ rats. The onset of massive, intraislet B- and T-cell infiltration in Lyp/Lyp rats was preceded by Rel B+ cells in and around the islets, followed by ED1+ monocytes/macrophages. Rel B+ cells were more frequent in the parafollicular cortex of pancreatic lymph nodes from Lyp/Lyp than from Lyp/+ and +/+ rats. In the Lyp/Lyp thymus, we found significantly increased expression of IL-12p40 messenger RNA (mRNA; p < 0.001), located in the Rel B-protein-rich corticomedullary junction. The NF-κB/Rel B complex specifically transactivates genes involved in antigen presentation in dendritic cells. Rel B+ cells in the islets may therefore mark the onset of autoimmune insulitis and antigen-specific activation of autoreactive T cells in the lymph nodes of diabetes prone Lyp/Lyp BB rats. In the thymus, Rel B+ cells may support the Lyp-dependent development of self-reactive thymocytes by activation of cytokine expression.
(Less)
- author
- Bieg, Sabine
; Simonson, William T
; Ellefsen, Kristian
and Lernmark, Åke
LU
- publishing date
- 2000-01
- type
- Contribution to journal
- publication status
- published
- keywords
- Antigen-presenting cell, Congenic, Dendritic cell, Diabetes, Pancreas, T cell
- in
- Pancreas
- volume
- 20
- issue
- 1
- pages
- 8 pages
- publisher
- Lippincott Williams & Wilkins
- external identifiers
-
- pmid:10630383
- scopus:0033957431
- ISSN
- 0885-3177
- DOI
- 10.1097/00006676-200001000-00007
- language
- English
- LU publication?
- no
- id
- 53f0b0d1-8368-4d4b-b52c-caec02257fd9
- date added to LUP
- 2017-09-06 15:21:33
- date last changed
- 2024-03-17 20:38:18
@article{53f0b0d1-8368-4d4b-b52c-caec02257fd9,
abstract = {{<p>Because the development of insulitis and diabetes is predictable in Lyp/Lyp congenic BB rats, we have characterized early islet inflammation in these rats to determine the cell subsets involved in the onset of autoimmune insulitis. Pancreas sections from prediabetic Lyp/Lyp, Lyp/+ and +/+ rats were analyzed by immunohistochemistry. We found W3/25+ cells in the exo- and endocrine tissue from all three genotypes, but intraislet insulitis was never found in Lyp/+ or +/+ rats. The onset of massive, intraislet B- and T-cell infiltration in Lyp/Lyp rats was preceded by Rel B+ cells in and around the islets, followed by ED1+ monocytes/macrophages. Rel B+ cells were more frequent in the parafollicular cortex of pancreatic lymph nodes from Lyp/Lyp than from Lyp/+ and +/+ rats. In the Lyp/Lyp thymus, we found significantly increased expression of IL-12p40 messenger RNA (mRNA; p < 0.001), located in the Rel B-protein-rich corticomedullary junction. The NF-κB/Rel B complex specifically transactivates genes involved in antigen presentation in dendritic cells. Rel B+ cells in the islets may therefore mark the onset of autoimmune insulitis and antigen-specific activation of autoreactive T cells in the lymph nodes of diabetes prone Lyp/Lyp BB rats. In the thymus, Rel B+ cells may support the Lyp-dependent development of self-reactive thymocytes by activation of cytokine expression.</p>}},
author = {{Bieg, Sabine and Simonson, William T and Ellefsen, Kristian and Lernmark, Åke}},
issn = {{0885-3177}},
keywords = {{Antigen-presenting cell; Congenic; Dendritic cell; Diabetes; Pancreas; T cell}},
language = {{eng}},
number = {{1}},
pages = {{47--54}},
publisher = {{Lippincott Williams & Wilkins}},
series = {{Pancreas}},
title = {{Rel B is an early marker of autoimmune islet inflammation in the BioBreeding (BB) rat}},
url = {{http://dx.doi.org/10.1097/00006676-200001000-00007}},
doi = {{10.1097/00006676-200001000-00007}},
volume = {{20}},
year = {{2000}},
}