ArticleThe Journal of experimental medicine1993
Thymic T cell anergy in autoimmune nonobese diabetic mice is mediated by deficient T cell receptor regulation of the pathway of p21ras activation.
Article in The Journal of experimental medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 93 citations in OpenAlex.
- Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice.Mediators of inflammation · 2018Article
- Thymic negative selection is functional in NOD mice.The Journal of experimental medicine · 2012Article
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- Antigen-Experienced CD4lo T Cells Are Linked to Deficient Contraction of the Immune Response in Autoimmune Diabetes.Autoimmune diseases · 2010Article
- Quantitative phosphoproteomic analysis of T cell receptor signaling in diabetes prone and resistant mice.Journal of proteome research · 2010Article
- Evidence for aberrant regulation of MAP kinase signal transduction pathway in peripheral blood mononuclear cells in patients with active celiac disease.Digestive diseases and sciences · 2009Article
- Autologous umbilical cord blood infusion for type 1 diabetes.Experimental hematology · 2008Review
- DNA vaccination with an insulin construct and a chimeric protein binding to both CTLA4 and CD40 ameliorates type 1 diabetes in NOD mice.Gene therapy · 2005Article
- Animal models of spontaneous autoimmune diabetes: notes on their relevance to the human disease.Current diabetes reports · 2004Review
- Ageing, autoimmunity and arthritis: Perturbations of TCR signal transduction pathways with ageing - a biochemical paradigm for the ageing immune system.Arthritis research & therapy · 2003Review
- Small GTPases in lymphocyte biology: Rho proteins take center stage.Immunologic research · 1999Review
- Neonatal activation of CD28 signaling overcomes T cell anergy and prevents autoimmune diabetes by an IL-4-dependent mechanism.The Journal of clinical investigation · 1997Article
- Impaired plasma membrane targeting of Grb2-murine son of sevenless (mSOS) complex and differential activation of the Fyn-T cell receptor (TCR)-zeta-Cbl pathway mediate T cell hyporesponsiveness in autoimmune nonobese diabetic mice.The Journal of experimental medicine · 1997Article
- Lactogenic hormones rapidly activate p21( ras )/mitogen-activated protein kinase in Nb2-11C rat lymphoma cells.Endocrine · 1996Article
- A protective role of gamma delta T cells in primary infection with Listeria monocytogenes in autoimmune non-obese diabetic mice.Immunology · 1995Article
- Interleukin-4: new diabetes champion?CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 1994Article
- p21ras and calcineurin synergize to regulate the nuclear factor of activated T cells.The Journal of experimental medicine · 1993Article
- Antigen-induced B lymphocyte activation involves the p21ras and ras.GAP signaling pathway.The Journal of experimental medicine · 1993Article
- Interleukin 4 reverses T cell proliferative unresponsiveness and prevents the onset of diabetes in nonobese diabetic mice.The Journal of experimental medicine · 1993Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thymic T cell anergy, as manifested by thymocyte proliferative unresponsiveness to antigens expressed in the thymic environment, is commonly believed to mediate the acquisition of immunological self-tolerance. However, we previously found that thymic T cell anergy may lead to the breakdown of tolerance and predispose to autoimmunity in nonobese diabetic (NOD) mice. Here, we show that NOD thymic T cell anergy, as revealed by proliferative unresponsiveness in vitro after stimulation through the T cell receptor (TCR), is associated with defective TCR-mediated signal transduction along the PKC/p21ras/p42mapk pathway of T cell activation. PKC activity is reduced in NOD thymocytes. Activation of p21ras is deficient in quiescent and stimulated NOD T cells, and this is correlated with a significant reduction in the tyrosine phosphorylation of p42mapk, a serine/threonine kinase active downstream of p21ras. Treatment of NOD T cells with a phorbol ester not only enhances their p21ras activity and p42mapk tyrosine phosphorylation but also restores their proliferative responsiveness. Since p42mapk activity is required for progression through to S phase of the cell cycle, our data suggest that reduced tyrosine phosphorylation of p42mapk in stimulated NOD T cells may abrogate its activity and elicit the proliferative unresponsiveness of these cells.
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