ArticleDiabetologia2005
Homing of human autoreactive T cells into pancreatic tissue of NOD-scid mice.
Article in Diabetologia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Mucosal Addressin Cell Adhesion Molecule-1 Mediates T Cell Migration into Pancreas-Draining Lymph Nodes for Initiation of the Autoimmune Response in Type 1 Diabetes.International journal of molecular sciences · 2024Article
- The beta cell-immune cell interface in type 1 diabetes (T1D).Molecular metabolism · 2023Review
- T1D progression is associated with loss of CD3Nature metabolism · 2020Article
- The development of human immune system mice and their use to study tolerance and autoimmunity.Journal of translational autoimmunity · 2019Review
- Article
- The importance of the Non Obese Diabetic (NOD) mouse model in autoimmune diabetes.Journal of autoimmunity · 2016Review
- Immune modulation in humans: implications for type 1 diabetes mellitus.Nature reviews. Endocrinology · 2014Review
- Regulatory multitasking of tolerogenic dendritic cells - lessons taken from vitamin d3-treated tolerogenic dendritic cells.Frontiers in immunology · 2013Article
- Nonviral delivery of small interfering RNA into pancreas-associated immune cells prevents autoimmune diabetes.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Advancing animal models of human type 1 diabetes by engraftment of functional human tissues in immunodeficient mice.Cold Spring Harbor perspectives in medicine · 2012Review
- The problems and promises of research into human immunology and autoimmune disease.Nature medicine · 2012Article
- Article
- Article
- An update on the use of NOD mice to study autoimmune (Type 1) diabetes.Expert review of clinical immunology · 2010Article
- Specific gene expression signature associated with development of autoimmune type-I diabetes using whole-blood microarray analysis.Genes and immunity · 2010Article
- Islet inflammation and CXCL10 in recent-onset type 1 diabetes.Clinical and experimental immunology · 2010Article
- The target cell response to cytokines governs the autoreactive T cell repertoire in the pancreas of NOD mice.Diabetologia · 2009Article
- The CXCR4/CXCL12 (SDF-1) signalling pathway protects non-obese diabetic mouse from autoimmune diabetes.Clinical and experimental immunology · 2007Article
Corrections and comments
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisAn important prerequisite for the initiation of pancreatic islet inflammation is the recruitment of pathogenic T cells. We investigated the in vivo migration patterns of human islet-reactive T cell clones after transfer into compromised hosts.
methodsNOD-scid mice were injected with a mixture of human autoreactive T cells and antigen-presenting cells. Survival and migration of T cells was analysed by fluorescence-activated cell sorter and immunohistochemical analysis of various tissues.
resultsAutoreactive T cells and antigen-presenting cells survived at least 14 days in vivo and accumulated in spleen, pancreatic tissue and pancreas draining lymph nodes, but not elsewhere, as early as 4 days after transfer. This homing was dependent on co-injection of human antigen-presenting cells loaded with autoantigen. Finally, we found that this process is enhanced by streptozotocin treatment. Streptozotocin treatment did not affect the constitutive homing to pancreas draining lymph nodes. Histological analysis of pancreatic tissue sections showed some autoreactive T cells around the islets of Langerhans, comparable to early peri-islet insulitis. However, the majority of pancreas-infiltrating T cells accumulated around blood vessels in the exocrine pancreas. All T cell clones expressed the chemokine receptor CXCR3 that is associated with homing to insulitic lesions in men and mice. CONCLUSIONS/
interpretationOur study provides the first evidence of in vivo accumulation in pancreatic tissue of islet-reactive T cells derived from type 1 diabetic patients. The fact that such T cells do not penetrate islets is in line with the concept that additional factors may be required for the entry of T cells into inflamed islets to become diabetogenic.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.