{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Loftus SN"],"funding":["National Institute of Arthritis and Musculoskeletal and Skin Diseases","NIDDK NIH HHS","George M. O'Brien Michigan Kidney Translational Core Center","NIAMS NIH HHS","Arthritis National Research Foundation"],"pagination":["1162799"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10227599"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14"],"pubmed_abstract":["Aberrant activation of the innate immune system is a known driver of lupus pathogenesis. Inhibition of the inflammasome and its downstream signaling components in murine models of lupus has been shown to reduce the severity of disease. Interleukin-1 beta (IL-1β) is a proinflammatory cytokine released from cells following inflammasome activation. Here, we examine how loss of IL-1β affects disease severity in the lupus-prone NZM2328 mouse model. We observed a sex-biased increase in immune complex deposition in the kidneys of female mice in the absence of IL-1β that corresponds to worsened proteinuria. Loss of IL-1β did not result in changes in overall survival, anti-dsDNA autoantibody production, or renal immune cell infiltration. RNA-sequencing analysis identified upregulation of TNF and IL"],"journal":["Frontiers in immunology"],"pubmed_title":["Loss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model."],"pmcid":["PMC10227599"],"funding_grant_id":["R01-AR071384 , K24AR076975, K01AR072129, UC2 AR081033, P30AR075043","R01 AR071384","P30DK081943","P30 DK081943","UC2 AR081033","K01 AR072129","P30 AR075043","K24 AR076975"],"pubmed_authors":["Kahlenberg JM","Liu J","Berthier CC","Gudjonsson JE","Loftus SN","Tsoi LC","Gharaee-Kermani M"],"additional_accession":[]},"is_claimable":false,"name":"Loss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model.","description":"Aberrant activation of the innate immune system is a known driver of lupus pathogenesis. Inhibition of the inflammasome and its downstream signaling components in murine models of lupus has been shown to reduce the severity of disease. Interleukin-1 beta (IL-1β) is a proinflammatory cytokine released from cells following inflammasome activation. Here, we examine how loss of IL-1β affects disease severity in the lupus-prone NZM2328 mouse model. We observed a sex-biased increase in immune complex deposition in the kidneys of female mice in the absence of IL-1β that corresponds to worsened proteinuria. Loss of IL-1β did not result in changes in overall survival, anti-dsDNA autoantibody production, or renal immune cell infiltration. RNA-sequencing analysis identified upregulation of TNF and IL","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023","modification":"2026-05-29T14:01:54.475Z","creation":"2024-11-13T04:03:46.148Z"},"accession":"S-EPMC10227599","cross_references":{"pubmed":["37261358"],"doi":["10.3389/fimmu.2023.1162799"]}}