Open AccessLocal production and localization of transforming growth factor‐beta in tuberculous pleurisy
Author(s) -
MAEDA J.,
UEKI N.,
OHKAWA T.,
IWAHASHI N.,
NAKANO T.,
HADA T.,
HIGASHINO K.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb05944.x
Subject(s) - pleurisy , immunology , beta (programming language) , medicine , transforming growth factor beta , production (economics) , tuberculosis , transforming growth factor , pleural effusion , pathology , computer science , economics , macroeconomics , programming language
SUMMARY Transforming growth factor‐beta (TGF‐β) is one of the cytokines which play an immunosuppressive role in an inflammatory process. To investigate the local production of TGF‐β, we evaluated the levels of TGF‐β in tuberculous pleural effusions (TBPE) and non‐tuberculous benign pleural effusions (non‐TBPE) by the growth inhibition assay with MvILu mink lung epithelial cells. The mean level of TGF‐β in TBPE (46.1 ± 31.5 pM; mean ± s.d.) was higher than in non‐TBPE (21.7 ± 12.3 pM) ( P <0.05). Although the level of interferon‐gamma (IFN‐γ) in TBPE measured by ELISA was significantly higher than in non‐TBPE. there was no significant difference in the levels of tumour necrosis factor‐alpha (TNF‐α) measured by ELISA between these two groups. Moreover, to elucidate localization of TGF‐β in tuberculous pleurisy, immunohistochemical studies of pleura, using the rabbit polyclonal antibody Ab39 against latent TGF‐β1 binding protein (LTBP) were performed. Results revealed that LTBP was localized in immature fibrotic areas where infiltrations of T lymphocytes and macrophages were absent. Importantly, the major sources of LTBP in these areas were thought to be mesothelial cells and fibroblasts. LTBP was not found in granulomas and mature fibrotic areas. Our data suggest that TGF‐β in tuberculous pleurisy may play important roles for regression of granulomatous inflammation and pleural fibrosis for tissue repair.