{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yin R"],"funding":["Ragon Institute of MGH, MIT and Harvard (Ragon Institute)","Massachusetts Institute of Technology","Massachusetts Institute of Technology (MIT)","Ragon Institute of MGH, MIT and Harvard","National Science Foundation (NSF)","National Science Foundation"],"pagination":["e2318599121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10945823"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(11)"],"pubmed_abstract":["T cells help orchestrate immune responses to pathogens, and their aberrant regulation can trigger autoimmunity. Recent studies highlight that a threshold number of T cells (a quorum) must be activated in a tissue to mount a functional immune response. These collective effects allow the T cell repertoire to respond to pathogens while suppressing autoimmunity due to circulating autoreactive T cells. Our computational studies show that increasing numbers of pathogenic peptides targeted by T cells during persistent or severe viral infections increase the probability of activating T cells that are weakly reactive to self-antigens (molecular mimicry). These T cells are easily re-activated by the self-antigens and contribute to exceeding the quorum threshold required to mount autoimmune responses"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["How persistent infection overcomes peripheral tolerance mechanisms to cause T cell-mediated autoimmune disease."],"pmcid":["PMC10945823"],"funding_grant_id":["Physics of Living Systems Fellowship","2141064","220568","DMR-2218849"],"pubmed_authors":["Melton S","Huseby ES","Chakraborty AK","Yin R","Kardar M"],"additional_accession":[]},"is_claimable":false,"name":"How persistent infection overcomes peripheral tolerance mechanisms to cause T cell-mediated autoimmune disease.","description":"T cells help orchestrate immune responses to pathogens, and their aberrant regulation can trigger autoimmunity. Recent studies highlight that a threshold number of T cells (a quorum) must be activated in a tissue to mount a functional immune response. These collective effects allow the T cell repertoire to respond to pathogens while suppressing autoimmunity due to circulating autoreactive T cells. Our computational studies show that increasing numbers of pathogenic peptides targeted by T cells during persistent or severe viral infections increase the probability of activating T cells that are weakly reactive to self-antigens (molecular mimicry). These T cells are easily re-activated by the self-antigens and contribute to exceeding the quorum threshold required to mount autoimmune responses","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-22T05:34:39.839Z","creation":"2024-11-15T04:37:01.848Z"},"accession":"S-EPMC10945823","cross_references":{"pubmed":["38446856"],"doi":["10.1073/pnas.2318599121"]}}