Abstract
Systemic inflammation is a feature of chronic obstructive pulmonary disease (COPD). Defects in T cell-mediated anti-inflammatory pathways such as cytotoxic T lymphocyte antigen-4 (CTLA-4) may promote damaging inflammation. This study provides novel data implicating the impaired induction of an anti-inflammatory molecule, CTLA-4 in the elevated inflammation observed in COPD patients. Low induction of CTLA-4 in COPD patients paralleled increased markers of systemic inflammation ex vivo and increased T-cell responses to a bacterial superantigen, staphylococcal enterotoxin-B (SEB) in vitro. This mechanism may explain the increased inflammation in COPD patients.
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