{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tanaka T"],"funding":["Research Core of Ocular Physiopathology and Therapeutics from University of São Paulo","Intramural NIH HHS","Conselho Nacional de Desenvolvimento Científico e Tecnológico","Division of Intramural Research, NIDCR/NIH","JSPS Research Fellowship for Japanese Biomedical and Behavioral Researchers at NIH","Fundação de Amparo a Pesquisa do Estado de São Paulo"],"pagination":["15169"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7494869"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_abstract":["Primary Sjögren's syndrome (pSS) is a complex autoimmune disease characterized by dysfunction of secretory epithelia with only palliative therapy. Patients present with a constellation of symptoms, and the diversity of symptomatic presentation has made it difficult to understand the underlying disease mechanisms. In this study, aggregation of unbiased transcriptome profiling data sets of minor salivary gland biopsies from controls and Sjögren's syndrome patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-LAMP) in a subset of Sjögren's syndrome cases. Stratification of patients based on their clinical characteristics suggested an association between increased LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-nuclear antibodies. In vitro studies demonstrated that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis. Interestingly, LAMP3 expression resulted in the accumulation and release of intracellular TRIM21 (one component of SSA), La (SSB), and α-fodrin protein, common autoantigens in Sjögren's syndrome, via extracellular vesicles in an apoptosis-independent mechanism. This study defines a clear role for LAMP3 in the initiation of apoptosis and an independent pathway for the extracellular release of known autoantigens leading to the formation of autoantibodies associated with this disease.ClinicalTrials.gov Identifier: NCT00001196, NCT00001390, NCT02327884."],"journal":["Scientific reports"],"pubmed_title":["LAMP3 induces apoptosis and autoantigen release in Sjogren's syndrome patients."],"pmcid":["PMC7494869"],"funding_grant_id":["2014/23211-0","71713","ZIA DE000695","302355/2017-0","12.1.25431.01.7","1ZIADE000695"],"pubmed_authors":["Odani T","Motta ACF","Rocha EM","Suizu F","Atsumi T","Mo YQ","Nakamura H","Warner BM","Noguchi M","Chiorini JA","Oliveira FR","Yin H","Hirata N","Ishigaki S","Jang SI","Tanaka T","Michael DG","Ji Y","Ribeiro-Silva A"],"additional_accession":[]},"is_claimable":false,"name":"LAMP3 induces apoptosis and autoantigen release in Sjogren's syndrome patients.","description":"Primary Sjögren's syndrome (pSS) is a complex autoimmune disease characterized by dysfunction of secretory epithelia with only palliative therapy. Patients present with a constellation of symptoms, and the diversity of symptomatic presentation has made it difficult to understand the underlying disease mechanisms. In this study, aggregation of unbiased transcriptome profiling data sets of minor salivary gland biopsies from controls and Sjögren's syndrome patients identified increased expression of lysosome-associated membrane protein 3 (LAMP3/CD208/DC-LAMP) in a subset of Sjögren's syndrome cases. Stratification of patients based on their clinical characteristics suggested an association between increased LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-nuclear antibodies. In vitro studies demonstrated that LAMP3 expression induces epithelial cell dysfunction leading to apoptosis. Interestingly, LAMP3 expression resulted in the accumulation and release of intracellular TRIM21 (one component of SSA), La (SSB), and α-fodrin protein, common autoantigens in Sjögren's syndrome, via extracellular vesicles in an apoptosis-independent mechanism. This study defines a clear role for LAMP3 in the initiation of apoptosis and an independent pathway for the extracellular release of known autoantigens leading to the formation of autoantibodies associated with this disease.ClinicalTrials.gov Identifier: NCT00001196, NCT00001390, NCT02327884.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Sep","modification":"2024-11-08T09:10:39.209Z","creation":"2020-09-21T07:01:25Z"},"accession":"S-EPMC7494869","cross_references":{"pubmed":["32939030"],"doi":["10.1038/s41598-020-71669-5"]}}