BackgroundPatients with systemic lupus erythematosus (SLE) often develop age-related adverse outcomes at a young age, raising the possibility that immune-aging processes may interact with chronic immune activation, treatment exposure, and accumulated damage in shaping long-term disease burden. Although immune-age acceleration has also been reported in rheumatoid arthritis and chronic viral infections (e.g., HIV/CMV), SLE is particularly well suited as a human model of inflammation-driven immune aging because of its typical onset in young women and the convergence of aging signatures across clinical, cellular, and molecular levels.Main bodyThis review synthesizes evidence for accelerated immunosenescence in SLE across systemic manifestations, immune cell remodeling, and molecular senescence markers.
Clinically, SLE is linked to premature cardiovascular disease, frailty, cognitive impairment, severe infections, and reduced vaccine responsiveness. Immunologically, senescent-like immune subsets (including terminally differentiated T cells, age-associated/double-negative B cells, dysfunctional NK cells, and senescence-like myeloid cells) expand prematurely.
Molecular features include inflammaging-like cytokine patterns, telomere attrition, and epigenetic age acceleration.
Frontiers in Immunology published a clinical update in Infectious Disease on 17 Jun 2026.
The item focuses on Accelerated immunosenescence in SLE: current evidence and clinical translation.
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