[Interleukin-2 receptor expression in pulmonary granulomatous diseases].
Interleukin-2 receptor expression (IL-2R) on monocytes and alveolar macrophages (AM) was determined in patients with sarcoidosis and pulmonary tuberculosis. In sarcoidosis and tuberculosis, IL-2R on monocytes was detectable, while it was undetectable in healthy controls. IL-2R on AM in sarcoidosis and tuberculosis was significantly increased as compared to healthy controls. IFN-gamma, which has been shown to be increased in sarcoidosis and tuberculosis as compared to healthy controls, induced IL-2R on monocytes in healthy controls, suggesting that IFN-gamma is at least in part responsible for the induction or enhancement of IL-2R on monocytes or AM in sarcoidosis and tuberculosis. Phorbol myristate acetate which is known to be protein kinase C (PKC) activator induced IL-2R on monocytes, and PKC inhibitor, H7, inhibited IFN-gamma-induced IL-2R on monocytes in healthy controls. Calcium ionophore, A23187, induced IL-2R on monocytes and calmodulin antagonist, W7, inhibited IFN-gamma-induced IL-2R on monocytes. Based on these results, it seems that not only the PKC pathway but also the calcium-calmodulin pathway is involved in IFN-gamma-induced IL-2R.
Ina
Y
Y
Second Department of Internal Medicine, Nagoya City University Medical School.
Takada
K
K
Miyachi
A
A
Noda
M
M
Sato
T
T
Hashiba
H
H
Ito
S
S
Iijima
N
N
Yamamoto
M
M
Morishita
M
M
D000328:Adult; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology; D008171:Lung Diseases / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology; D015375:Receptors, Interleukin-2 / Q000378:metabolism*; D012507:Sarcoidosis / Q000378:metabolism*; D015398:Signal Transduction; D014397:Tuberculosis, Pulmonary / Q000378:metabolism*
D015375:Receptors, Interleukin-2; D007371:Interferon-gamma