T-cell hyperreactivity might have a central role in the pathogenesis of progressive systemic sclerosis (PSS). By use of monoclonal antibodies directed against functional T-cell surface structures enhanced responsiveness to signals transmitted by the T-cell receptor pathway (CD3) and by accessory (CD28) molecules can be demonstrated. It remains to be elucidated whether increased monocyte function, disturbed intracellular signalling, or altered regulation of transcription might contribute to increased T-cell reactivity in patients with PSS.