Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Negative or inhibitory costimulatory pathways regulate T cell activation and play a role in peripheral tolerance. Targeting these pathways harnesses the physiologic mechanisms of regulating autoimmunity and could prove beneficial for the therapy of autoimmune diseases. However, attempts at targeting these pathways have been fraught with difficulties. In this issue of the JCI, Fife et al. describe a creative approach for targeting CTL-associated antigen 4 (CTLA-4) on activated T cells via genetically engineered B cells to prevent autoimmune diabetes in the NOD mouse (see the related article beginning on page 2252). Novel "designer" strategies targeting negative costimulatory pathways provide reasons for optimism in the search for a cure for devastating autoimmune diseases.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1523390 | PMC |
| http://dx.doi.org/10.1172/JCI29455 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Type I interferon limits central nervous system autoimmunity by modulating the microRNA-21-FOXO1 axis in pathogenic T helper 17 cells.
Sci Transl Med
September 2025
Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
IFN-β, a type I interferon, has been used as a first-line therapy for patients with multiple sclerosis (MS) for more than 30 years; however, the cellular and molecular basis of its therapeutic efficacy remains unclear. Here, we first used experimental autoimmune encephalomyelitis (EAE), a mouse model for MS, to show that the therapeutic effects of IFN-β were associated with a down-regulation of microRNA-21 (miR-21) and pathogenic T17 (pT17) cells. In vitro experiments demonstrated that genetic knockout of miR-21 directly inhibited pathogenic T17 cell differentiation.
View Article and Find Full Text PDFDevelopment of high-affinity peptide probes for improved diagnosis of Hashimoto's thyroiditis.
Mol Biol Rep
September 2025
Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Lysosome-dependent cell death: disease implications and potential therapeutic targets.
Mol Biol Rep
September 2025
School of Pharmacy, Heilongjiang University of Chinese Medicine, NO 24 Heping Road, 150040, Harbin, P. R. China.
Lysosome-dependent cell death (LDCD) is a regulated form of cell death initiated by increased lysosomal membrane permeability, leading to the cytoplasmic release of lysosomal enzymes and subsequent cellular damage. Molecular mechanisms controlling LDCD include lysosomal membrane instability and lysosomal enzyme release, which together lead to cell damage. A more profound comprehension of these underlying mechanisms may reveal new therapeutic targets for diseases associated with lysosomal dysfunction.
View Article and Find Full Text PDFHuman cytomegalovirus infection coopts chromatin organization to diminish TEAD1 transcription factor activity.
Elife
September 2025
Center for Autoimmune Genomics and Etiology, Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Human cytomegalovirus (HCMV) infects up to 80% of the world's population. Here, we show that HCMV infection leads to widespread changes in human chromatin accessibility and chromatin looping, with hundreds of thousands of genomic regions affected 48 hr after infection. Integrative analyses reveal HCMV-induced perturbation of Hippo signaling through drastic reduction of TEAD1 transcription factor activity.
View Article and Find Full Text PDFAdult onset cryopyrin-associated periodic syndrome due to germline missense mutation in in a previously healthy middle-aged woman.
Front Immunol
September 2025
Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea.
Background: Cryopyrin-associated periodic syndrome (CAPS) is an autoinflammatory disease caused by a gain-of-function mutation in the gene, which regulates inflammasome-mediated interleukin-1β (IL-1β) production. This leads to recurrent episodes of fever, rash, and arthritis, typically beginning in childhood.
Objective: To demonstrate the role of a missense mutation, c.