[Autoimmunity and ageing : How immune ageing shapes disease phenotype, infection risk and treatment safety in rheumatic diseases].

Immune ageing alters tolerance mechanisms, the chronic low-grade inflammatory environment and host infection defence. This is clinically relevant in rheumatology because the number of older patients with inflammatory rheumatic diseases is increasing and age modifies disease phenotype, vaccination responses and treatment safety. To summarize the interfaces between ageing, autoimmunity and chronic inflammation and to derive consequences for prevention and treatment. Narrative review of recent reviews and key studies on immunosenescence, geroscience, autoimmunity, infection risk, vaccination responses and translational biomarkers. Key features include loss of naïve lymphocytes, repertoire contraction, inflammaging, myeloid dysregulation and disorders of cellular homeostasis. Classical autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) show features of premature immune ageing, whereas giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) illustrate age-restricted inflammatory disease. Clinically, immune ageing translates into altered susceptibility to infection, weaker responses to vaccination and a narrower safety margin during immunosuppression. Age should be regarded as a biological modifier in rheumatic diseases. Clinical implications include early vaccination and infection prevention, glucocorticoid-sparing treatment strategies and biomarker-guided approaches that capture immunological rather than chronological age.