Abstract | BACKGROUND AND AIM OF THE WORK: Active sarcoidosis is considered to be a Th1 dominant condition. We examined whether Th1 cytokines are highly expressed at inflammed lesions of Japanese patients with sarcoidosis. METHODS: To investigate the mRNA expression of Th1 cytokines and IL-12 in sarcoid BAL cells, we used semiquantitative reverse transcription--polymerase chain reaction method. RESULTS: The mRNA expressions of Th1 cytokines (IFN-gamma and IL-2) in active sarcoid BAL cells were significantly elevated as compared with those in healthy volunteers. The proportion of positive IL-4 mRNA expression in sarcoid BAL cells was not significantly higher than that in healthy volunteers. Further, there was no significant difference in IFN-gamma mRNA levels between the groups positive and negative for IL-4 mRNA expression. Although the proportion of positive expression of IL-12 mRNA in active sarcoid BAL cells was not significantly higher than that in healthy volunteers, the group positive for IL-12 mRNA expression had significantly elevated levels of IFN-gamma mRNA than did the negative group. CONCLUSIONS: These results may indicate that IL-12 induces IFN-gamma expression and subsequent Th1 dominant condition in Japanese patients with sarcoidosis.
|
Authors | K Shigehara, N Shijubo, M Ohmichi, S Kon, Y Shibuya, R Takahashi, S Morita-Ichimura, T Tatsuno, Y Hiraga, S Abe, N Sato |
Journal | Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG
(Sarcoidosis Vasc Diffuse Lung Dis)
Vol. 17
Issue 2
Pg. 151-7
(Jun 2000)
ISSN: 1124-0490 [Print] Italy |
PMID | 10957763
(Publication Type: Comparative Study, Journal Article)
|
Chemical References |
- RNA, Messenger
- Interleukin-12
- Interferon-gamma
|
Topics |
- Adult
- Bronchoalveolar Lavage
- Cell Culture Techniques
- Female
- Gene Expression Regulation
- Humans
- Interferon-gamma
(biosynthesis, genetics)
- Interleukin-12
(pharmacology)
- Male
- Middle Aged
- RNA, Messenger
(biosynthesis)
- Reverse Transcriptase Polymerase Chain Reaction
- Sarcoidosis, Pulmonary
(genetics, immunology)
- T-Lymphocytes, Helper-Inducer
(immunology)
|