Lupus

Disease / Phenomenon

Systemic lupus erythematosus is a chronic autoimmune disease in which the immune system attacks the body's own tissues, producing inflammation that can affect almost any organ. Its presentation is famously variable: joint pain and swelling, the characteristic malar rash across the cheeks and nose, photosensitivity, mouth ulcers, fatigue, fever, hair loss, pleuritis or pericarditis, kidney inflammation, hematologic abnormalities, and neuropsychiatric symptoms. The course typically alternates between flares and periods of relative quiet, and severity ranges from mild to organ-threatening, with lupus nephritis a principal determinant of long-term outcome. Lupus predominantly affects women of reproductive age and shows substantial variation in incidence and severity across ancestral groups.

The central abnormality is loss of tolerance to nuclear self-antigens. Impaired clearance of apoptotic cell debris exposes nuclear material; autoreactive B cells produce antinuclear, anti-double-stranded DNA, and anti-Smith antibodies; and resulting immune complexes deposit in tissue, activating complement and recruiting effector cells. Plasmacytoid dendritic cells sensing nucleic acids through TLR7 and TLR9 generate a sustained type I interferon signature that defines much of the disease's biology. Neutrophil extracellular traps, T follicular helper cell expansion, BAFF signaling, and NF-kB-driven cytokine production contribute. This page decomposes these processes into pathways and biomarkers.