Am. J. Respir. Cell Mol. Biol., Vol 16, No. 4, Apr 1997, 429-437.
Alveolar macrophages produce the Env protein of a human endogenous retrovirus, HERV-E 4-1, in a subgroup of interstitial lung diseases
N Tamura, A Iwase, K Suzuki, N Maruyama and S Kira
Department of Respiratory Medicine, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.
We investigated whether intraalveolar inflammatory cells such as alveolar
macrophages or lymphocytes produced the gene product of a type- C human
endogenous retrovirus (HERV), HERV-E 4-1, which might initiate an immune
response resulting in interstitial lung disease. We evaluated HERV-E 4-1
Env protein production by bronchoalveolar lavage fluid (BALF) cells and PBL
in 109 patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF), lung
cancer, and rheumatoid lung disease as well as 26 normal control
individuals. Production of HERV-E 4-1 Env protein by alveolar macrophages
was observed using indirect immunofluorescence in 3 IPF patients and 3
sarcoidosis patients (6/135). No peripheral blood lymphocytes showed HERV-E
4-1 Env protein production. Antibodies to HERV-E 4-1 Env protein were
detected in the BALF of all six patients by immunoblot analysis, while none
of the normal control individuals showed HERV-E 4-1 Env protein antibody in
the BALF. All examined BALF cells showed HERV-E 4-1 env mRNA transcript
expression by reverse transcription-polymerase chain reaction. No
significant influence of point mutation or DNA polymorphism on HERV-E 4- 1
Env protein production was recognized. In conclusion, local production of
HERV-E 4-1 Env protein and defective tolerance of HERV gene products with
resultant antibody production may contribute to the pathogenesis of IPF or
sarcoidosis in some patients.
