摘要
Systemic inflammation is a feature of chronic obstructive pulmo- nary disease （COPD）. Defects in T cell-mediated anti-inflamma- tory 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-inflam- matory 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, staphylo- coccal enterotoxin-B （SEB） in vitro. This mechanism may explain the increased inflammation in COPD patients.
Systemic inflammation is a feature of chronic obstructive pulmo- nary disease （COPD）. Defects in T cell-mediated anti-inflamma- tory 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-inflam- matory 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, staphylo- coccal enterotoxin-B （SEB） in vitro. This mechanism may explain the increased inflammation in COPD patients.
