Open AccessReduced expression of the αβ T‐cell antigen receptor
by alveolar T‐cells
Author(s) -
Yamaguchi E.,
Itoh A.,
Furuya K.,
Hizawa N.,
Ohnuma N.,
Kodama N.,
Kojima J.,
Kawakami Y.
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.13d20.x
Subject(s) - t cell receptor , cd8 , antigen , cd3 , immune system , immunology , t lymphocyte , t cell , bronchoalveolar lavage , cytotoxic t cell , biology , pulmonary alveolus , alveolar cells , flow cytometry , pathology , in vitro , microbiology and biotechnology , medicine , lung , respiratory disease , biochemistry
A previous study revealed that reduced expression (modulation) of the CD3 antigen is a common characteristic of alveolar T‐cells in health and disease. As CD3 molecules are noncovalently bound to T‐cell antigen receptors (TCR), it was hypothesized that modulation of TCR was also a feature of alveolar T‐cells. To demonstrate this, lymphocytes from bronchoalveolar lavage fluid were stained with an anti‐αβTCR antibody and analysed by flow cytometry. The expression of αβTCR by alveolar T‐cells was evaluated by calculating mean fluorescence intensity (MFI) and was compared with αβTCR expression by autologous blood T‐cells. As anticipated from a previous study, modulation of TCR was observed not only in healthy volunteers but also in patients with pulmonary sarcoidosis, other pulmonary diseases, and nonpulmonary diseases. There were no significant differences in MFI of alveolar T‐cells among the study groups. The degree of modulation assessed by the difference of MFI between blood and alveolar T‐cells was greater for CD4+ cells than for CD8+ cells owing to the higher MFI of CD4+ blood T‐cells. Coculture of alveolar macrophages with blood T‐cells in vitro induced partial modulation of TCR. These results demonstrate the ubiquity of modulation of T‐cell receptors on alveolar T‐cells and suggest, in contrast to a previous report by other investigators that it is caused by some nonantigenic mechanism possibly inherent in the alveolar milieu. The implications of this phenomenon in in vivo immune responses of the lung need to be examined.