<b>Background:</b> Microvesicles (MVs) expressing the type 1 interferon (IFN)-inducible protein galectin-3 binding protein (G3BP) may play a pathogenic role in systemic lupus erythematosus (SLE).
<b>Background:</b> Microvesicles (MVs) expressing the type 1 interferon (IFN)-inducible protein galectin-3 binding protein (G3BP) may play a pathogenic role in systemic lupus erythematosus (SLE).
<b>Conclusion:</b> The results demonstrated a significant lower CAT and GSH levels and also revealed no significant difference for SOD and GPx levels in SLE patients.
<b>Conclusion:</b> The results demonstrated a significant lower CAT and GSH levels and also revealed no significant difference for SOD and GPx levels in SLE patients.
<b>Methods:</b> We measured the type I IFN score, derived from relative expressions of three IFN-inducible genes (MX-1, IFIT-1, and IFI-44) in peripheral blood mononuclear cells from 55 patients with PAPS, 34 with SLE/APS, 48 with SLE, and 28 controls.
<b>Methods:</b> We measured the type I IFN score, derived from relative expressions of three IFN-inducible genes (MX-1, IFIT-1, and IFI-44) in peripheral blood mononuclear cells from 55 patients with PAPS, 34 with SLE/APS, 48 with SLE, and 28 controls.
<b>Objective</b> To compare the risk of serious infections associated with use of systemic steroids, non-biologic agents, or tumor necrosis factor α (TNF) inhibitors in pregnancy.<b>Design</b> Observational cohort study.<b>Setting</b> Public (Medicaid, 2001-10) or private (Optum Clinformatics, 2004-15) health insurance programs in the US.<b>Participants</b> 4961 pregnant women treated with immunosuppressive drugs for rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, psoriatic arthritis, or inflammatory bowel disease.<b>Exposure for observational studies</b> Exposure was classified into steroid, non-biologic, or TNF inhibitors on first filled prescription during pregnancy.
<b>Objective:</b> Characterization of PTX3-specific (PTX3<sup>+</sup>) B cells in peripheral blood of SLE patients with or without LN and healthy donors (HD).
<b>Results:</b> Plasma IL-1β levels were unmodified in SLE respect to HC whereas IL-6 levels were higher in SLE than in HC, resulting significantly increased in SLE-S. Macrophages isolated from SLE patients released lower quantities of IL-1β after stimulation with BzATP, whereas IL-6 release was significantly augmented in SLE-NS respect to both HC and SLE-S after all types of stimulation.
<b>Results:</b> Plasma IL-1β levels were unmodified in SLE respect to HC whereas IL-6 levels were higher in SLE than in HC, resulting significantly increased in SLE-S. Macrophages isolated from SLE patients released lower quantities of IL-1β after stimulation with BzATP, whereas IL-6 release was significantly augmented in SLE-NS respect to both HC and SLE-S after all types of stimulation.
<i>IRF5</i> genetic risk has been widely replicated in systemic lupus erythematosus (SLE), and loss of <i>Irf5</i> ameliorates disease in murine lupus models, in part, through the lack of pathogenic autoantibody secretion.
<i>Conclusion.</i> Both IL-1<i>β</i> and IL-6 are highly expressed cytokines in RF+IgE+ SLE subtype which may be related to the pathogenesis of this special SLE subtype and provide accurate treatment strategy by neutralizing IL-1<i>β</i> and IL-6.