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 a...

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Published inNihon Kyōbu Shikkan Gakkai zasshi Vol. 29; no. 4; pp. 407 - 412
Main Authors Ina, Yasutaka, Takada, Katsutoshi, Miyachi, Atsuo, Noda, Masaharu, Sato, Toshihide, Hashiba, Hatsumi, Ito, Shinsuke, Iijima, Naoto, Yamamoto, Masahiko, Morishita, Munehiko, Yoshikawa, Kosho
Format Journal Article
LanguageJapanese
Published Japan The Japanese Respiratory Society 01.04.1991
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Summary: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-γ, 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-γ 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-γ-induced IL-2R on monocytes in healthy controls. Calcium ionophore, A23187, induced IL-2R on monocytes and calmodulin antagonist, W7, inhibited IFN-γ-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-γ-induced IL-2R.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
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ISSN:0301-1542
1883-471X
DOI:10.11389/jjrs1963.29.407