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© Research
Publication : Cell reports. Medicine

Inactive disease in patients with lupus is linked to autoantibodies to type I interferons that normalize blood IFNα and B cell subsets.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell reports. Medicine - 17 Jan 2023

Bradford HF, Haljasmägi L, Menon M, McDonnell TCR, Särekannu K, Vanker M, Peterson P, Wincup C, Abida R, Gonzalez RF, Bondet V, Duffy D, Isenberg DA, Kisand K, Mauri C,

Link to Pubmed [PMID] – 36652906

Link to DOI – 10089410.1016/j.xcrm.2022.100894S2666-3791(22)00473-6

Cell Rep Med 2023 Jan; 4(1): 100894

Systemic lupus erythematosus (SLE) is characterized by increased expression of type I interferon (IFN)-regulated genes in 50%-75% of patients. We report that out of 501 patients with SLE analyzed, 73 (14%) present autoantibodies against IFNα (anti-IFN-Abs). The presence of neutralizing-anti-IFN-Abs in 4.2% of patients inversely correlates with low circulating IFNα protein levels, inhibition of IFN-I downstream gene signatures, and inactive global disease score. Hallmarks of SLE pathogenesis, including increased immature, double-negative plasmablast B cell populations and reduction in regulatory B cell (Breg) frequencies, were normalized in patients with neutralizing anti-IFN-Abs compared with other patient groups. Immunoglobulin G (IgG) purified from sera of patients with SLE with neutralizing anti-IFN-Abs impedes CpGC-driven IFNα-dependent differentiation of B cells into immature B cells and plasmablasts, thus recapitulating the neutralizing effect of anti-IFN-Abs on B cell differentiation in vitro. Our findings highlight a role for neutralizing anti-IFN-Abs in controlling SLE pathogenesis and support the use of IFN-targeting therapies in patients with SLE lacking neutralizing-anti-IFN-Abs.