biostudies-literatureTumurkhuu GCedars-Sinai Leon Fine Translational Science AwardNIAID NIH HHSNational Institutes of HealthNIAMS NIH HHSNIH HHSCenter for Research in Women's Health Science, Cedars-Sinai172-183https://www.ebi.ac.uk/biostudies/studies/S-EPMC12326329biostudies-literatureUnknown78(1)<h4>Objective</h4>Patients with systemic lupus erythematosus (SLE) experience photosensitivity, with exposure to UVB light driving lupus flares and triggering symptoms like joint pain, fatigue, and cutaneous lesions. Although the mechanism(s) linking UVB exposure to systemic effects are unclear, type I interferons (IFNs) are known to play a role. Our previous work has shown that TRIM21, an autoantigen in SLE, functions as a negative regulator on the pathways driving IFN expression. Here we explore how TRIM21 functions to regulate both local and systemic inflammation following UVB exposure and how altered expression may drive cutaneous inflammation and photosensitivity in SLE.<h4>Methods</h4>Wild-type (WT; C57BL/6) and Trim21^-/- mice were irradiated with UVB (100 mJ/cm<sup>2</supArthritis & rheumatology (Hoboken, N.J.)Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.PMC12326329R01AI134030R56 AR0782791R56AR078279‐01A1R03HL15863R01 AI1340301R56AR078279-01A1Huo LNaveen Kumar AShon WStehlik CWallace DJJefferies CAForbess LMoore RDe Los Santos GOliver TCarriere JAbuav RTumurkhuu GAinsworth RIshimori MGibb DPerri GYu JMfalseLoss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.<h4>Objective</h4>Patients with systemic lupus erythematosus (SLE) experience photosensitivity, with exposure to UVB light driving lupus flares and triggering symptoms like joint pain, fatigue, and cutaneous lesions. Although the mechanism(s) linking UVB exposure to systemic effects are unclear, type I interferons (IFNs) are known to play a role. Our previous work has shown that TRIM21, an autoantigen in SLE, functions as a negative regulator on the pathways driving IFN expression. Here we explore how TRIM21 functions to regulate both local and systemic inflammation following UVB exposure and how altered expression may drive cutaneous inflammation and photosensitivity in SLE.<h4>Methods</h4>Wild-type (WT; C57BL/6) and Trim21^-/- mice were irradiated with UVB (100 mJ/cm<sup>2</sup2026-01-01T00:00:00Z2026 Jan2026-06-14T05:44:47.445Z2026-06-14T03:09:20.593ZS-EPMC123263294052434410.1002/art.43273