Lupus nephritis correlates with B cell interferon-β, anti-Smith, and anti-DNA: a retrospective study

Background In systemic lupus erythematosus (SLE), detection of interferon-β (IFNβ) in B cells was found to be most prominent in patients with high anti-Smith (Sm) and renal disease, but a mechanistic connection was not clear. The objective of the present study is to determine the association of IFNβ in peripheral blood naïve B cells with the histopathological features of lupus nephritis (LN). Methods The percentage of IFNβ + cells in IgD + CD27 − naïve CD19 + B cells (B cell IFNβ) among peripheral blood mononuclear cells (PBMCs) from 80 SLE patients were analyzed using flow cytometry. Serological and clinical data were collected. The correlations of B cell IFNβ with LN classification and with histopathological findings (light, electron, and immunofluorescence [IF] microscopic analyses for deposition of IgM, IgG, IgA, C1q, and C3) were determined in 23 available biopsy specimens. Results B cell IFNβ is positively associated with anti-Sm ( p = 0.001), anti-DNA ( p = 0.013), and LN ( p < 0.001) but was negatively associated with oral/nasal ulcer ( p = 0.003) and photosensitivity ( p = 0.045). B cell IFNβ positively correlated with immune complex (IC) deposit in the glomerular basement membrane (GBM) ( p = 0.002) but not in the mesangial ( p = 0.107) or tubular region ( p = 0.313). Patients with high B cell IFNβ had statistically increased development of the proliferative LN (Classes III, IV and/or V), compared to patients with low B cell IFNβ ( p < 0.0001). Histopathological features positively associated with increased B cell IFNβ included active glomerular lesions as determined by fibrocellular crescents ( p = 0.023), chronic glomerular lesions indicated by segmental sclerosis ( p = 0.033), and a membranous pattern of renal damage indicated by spike/holes ( p = 0.015). Conclusion B cell IFNβ correlates with history of severe LN, glomerular basement membrane (GBM) IC deposition, and anatomical features of both active and chronic glomerular lesions.