T-lymphocyte effector functions and signalling defects with ageing, role in autoimmune diseases. Defects in many activation pathways and molecules lead to differential effects on T-cell behaviour, and thus on immune responses. Membrane reorganization, cytokine profiles, cellular interactions, and T-cell subpopulation shifts are the consequences of the changes observed in T-cell signalling with ageing. The final consequence is an increased susceptibility to disease that is accompanied by the development of a local environment of a sustained inflammatory state, critical factors for the initiation, the development and the chronicity of autoimmune diseases. Abs, antibodies; AICD, activation-induced cell death; APC, antigen-presenting cell; ARD, autoimmune renal disease; CTLA-4, cytotoxic T-leukocyte antigen-4; ECM, extracellular matrix; FBL, fibroblast; ICOS, inducible costimulatory protein; IL-2R, IL-2 receptor; IP3, myoinositol 1,4,5-trisphosphate; LAT, linker of activated T cells; MΦ, macrophage; MAP, mitogen-activated protein; MMP, matrix metalloproteinase; PA, psoriasis arthritis; PKC, protein kinase C; RA, rheumatoid arthritis; SD, scleroderma; SLE, systemic lupus erythematosus; TCR, T-cell receptor.