Local Expression of TNFα in Neonatal NOD Mice Promotes Diabetes by Enhancing Presentation of Islet Antigens
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TLDR
It is demonstrated that islet-specific expression of TNFalpha in neonatal nonobese diabetic mice accelerated diabetes and inflammation can trigger autoimmunity by recruiting and activating dendritic cells/macrophages to present self-antigens to autoreactive T cells.About:
This article is published in Immunity.The article was published on 1998-11-01 and is currently open access. It has received 197 citations till now. The article focuses on the topics: Antigen-presenting cell & Interleukin 12.read more
Citations
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β-Cell death during progression to diabetes
TL;DR: The hallmark of type 1 diabetes is specific destruction of pancreatic islet β-cells, which is crucial at several points during disease progression, initiating leukocyte invasion of the islets and terminating the production of insulin in islet cells.
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Mast Cells Are Essential for Early Onset and Severe Disease in a Murine Model of Multiple Sclerosis
TL;DR: Reconstitution of the mast cell population in W/Wv mice restores induction of early and severe disease to wild-type levels, suggesting that mast cells are critical for the full manifestation of disease.
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Establishment of NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes
TL;DR: It is reported that PD-1 deficiency specifically accelerates the onset and frequency of type I diabetes in NOD (nonobese diabetic) mice, with strong T helper 1 polarization of T cells infiltrating into islets and leading to the induction of different forms of autoimmune diseases depending on the genetic background of the strain.
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Pancreatic Lymph Node-Derived CD4+CD25+ Treg Cells: Highly Potent Regulators of Diabetes that Require TRANCE-RANK Signals
TL;DR: It is shown in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans.
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Neonatal beta-cell apoptosis: a trigger for autoimmune diabetes?
Jacqueline D. Trudeau,Jan P. Dutz,Edith Arany,David J. Hill,Warren E. Fieldus,Diane T. Finegood +5 more
TL;DR: In this paper, the authors used both mathematical modeling and histochemical detection methods to demonstrate that β-cell apoptosis is significantly increased in neonates as compared with adult rats, peaking at approximately 2 weeks of age.
References
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Dendritic cells and the control of immunity
TL;DR: Once a neglected cell type, dendritic cells can now be readily obtained in sufficient quantities to allow molecular and cell biological analysis and the realization that these cells are a powerful tool for manipulating the immune system is realized.
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A conditioned dendritic cell can be a temporal bridge between a CD4 + T-helper and a T-killer cell
TL;DR: It is found that the three cells need not meet simultaneously but that the helper cell can first engage and ‘condition’ the dendritic cell, which then becomes empowered to stimulate a killer cell.
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Dendritic cells acquire antigen from apoptotic cells and induce class I-restricted CTLs
TL;DR: It is shown that human dendritic cells, but not macrophages, efficiently present antigen derived from apoptotic cells, stimulating class I-restricted CD8+ CTLs, suggesting a mechanism by which potent APCs acquire antigens from tumours, transplants, infected cells, or even self-tissue, for stimulation or tolerization of C TLs.
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Help for cytotoxic-T-cell responses is mediated by CD40 signalling
Sally R.M. Bennett,Sally R.M. Bennett,Francis R. Carbone,Freda Karamalis,Freda Karamalis,Richard A. Flavell,Jacques F. A. P. Miller,William R. Heath +7 more
TL;DR: It is shown that signalling through CD40 on the antigen-presenting cells can replace the requirement for TH cells, indicating that T-cell ‘help’, at least for generation of CTLs by cross-priming, is mediated by signalling throughCD40 onThe antigen- presenting cell.
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Protection from obesity-induced insulin resistance in mice lacking TNF-|[alpha]| function
TL;DR: Results indicate that TNF-α is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action.