Type I Interferon-Dependent and -Independent TRIF Signaling are Required for Autoantibody Generation in an Induced Model of Systemic Lupus Erythematosus

نویسندگان

چکیده

Abstract Systemic lupus erythematosus (SLE) is an autoimmune condition characterized by the production of autoantibodies to cellular and nuclear self-antigens, with damage multiple organs. Immunization SLE autoantigen β2-glycoprotein I (β2GPI) TLR4 ligand lipopolysaccharide (LPS) induces a murine model generation antigens. LPS both inflammatory cytokines type interferons (IFNs) signaling through adaptor proteins MyD88 TRIF, respectively. We investigated mechanisms LPS-dependent on induction following β2GPI/LPS immunization. mice deficient in or TRIF revealed that preferentially promoted autoantibody this model, compared signaling. Furthermore, SLE-specific was induced TLR3 agonists, combination β2GPI, but not agonists TRIF-independent TLRs. RNA-sequencing dendritic cells macrophages isolated from wildtype (WT) TRIF-deficient immunized differential expression IFN-dependent -independent genes. Moreover, IFN receptor (IFNaR)-deficient showed diminished WT mice, lesser extent than mice. conclude required for our - independent effects. Supported grants CIHR (????)

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.78.04