|
|
||||||||
1 Dept of Pneumology and Allergy, Ruhrlandklinik, Medical Faculty, University of Essen, Essen, and 2 General and Experimental Pathology, Ruhr University, Bochum, Germany. 3 Dept of General Medicine and Clinical Investigation, Nara Medical University, Nara, Japan
CORRESPONDENCE: U. Costabel, Ruhrlandklinik, Tüschener Weg 40, 45239 Essen, Germany. Fax: 49 2014334029. E-mail: erj.costabel@t-online.de
Keywords: Alveolar lymphocytes, alveolar macrophages, Fas receptors, hypersensitivity pneumonitis, tumour necrosis factor receptors 1 and 2
Received: July 16, 2004
Accepted February 4, 2005
Tumour necrosis factor receptors (TNFR) and the Fas receptor (FasR) have been implicated in the pathogenesis of interstitial lung diseases. The current authors examined the expression of TNFR-1, TNFR-2 and FasR by bronchoalveolar cells in hypersensitivity pneumonitis (HP).
Cell surface receptor expression on bronchoalveolar lavage cells was analysed by immunocytochemistry in 11 HP patients, 11 idiopathic pulmonary fibrosis (IPF) patients and 10 controls.
TNFR-1, TNFR-2 and FasR were expressed on a higher percentage of alveolar macrophages (AM) in HP compared with controls and IPF patients. TNFR-2 and FasR expression on lymphocytes was also higher in HP than in controls and in IPF. TNFR-1, TNFR-2 and FasR expression correlated positively with the percentage of lymphocytes, and negatively with the percentage of AM in HP. Expression of TNFR-1 on AM and TNFR-2 on lymphocytes correlated with the percentage of neutrophils in HP.
In conclusion, this study shows evidence of altered expression of tumour necrosis factor superfamily receptors in hypersensitivity pneumonitis.
This article has been cited by other articles:
![]() |
N. Khalil, A. Churg, N. Muller, and R. O'Connor Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis Toxicol Pathol, January 1, 2007; 35(1): 86 - 96. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |