Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.

ABSTRACT:

Objective

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.

Methods

Wild-type (WT; C57BL/6) and Trim21^-/- mice were irradiated with UVB (100 mJ/cm²

SUBMITTER: Tumurkhuu G 

PROVIDER: S-EPMC12326329 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature