biostudies-literatureLoftus SNNational Institute of Arthritis and Musculoskeletal and Skin DiseasesNIDDK NIH HHSGeorge M. O'Brien Michigan Kidney Translational Core CenterNIAMS NIH HHSArthritis National Research Foundation1162799https://www.ebi.ac.uk/biostudies/studies/S-EPMC10227599biostudies-literatureUnknown14Aberrant 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 ILFrontiers in immunologyLoss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model.PMC10227599R01-AR071384 , K24AR076975, K01AR072129, UC2 AR081033, P30AR075043R01 AR071384P30DK081943P30 DK081943UC2 AR081033K01 AR072129P30 AR075043K24 AR076975Kahlenberg JMLiu JBerthier CCGudjonsson JELoftus SNTsoi LCGharaee-Kermani MfalseLoss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model.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 IL2023-01-01T00:00:00Z20232026-05-29T14:01:54.475Z2024-11-13T04:03:46.148ZS-EPMC102275993726135810.3389/fimmu.2023.1162799