Monocyte/macrophage polypeptides (monokines) alter the properties of synovial cells. This interaction could explain some of the properties of the inflamed synovium in rheumatic disease. Only recently has it been possible to test the action of purified monokines on the target synovial cells. We repor
Differential expression of interleukin 1α by Thy-1+ and Thy-1− lung fibroblast subpopulations: Enhancement of interleukin 1α production by tumor necrosis factor-α
✍ Scribed by Richard P. Phipps; Clare Baecher; John G. Frelinger; David P. Penney; Peter Keng; Deborah Brown
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 535 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Differential expression of interleukin la by Thy-l+ and Thy-llung fibroblast subpopulations: enhancement of interleukin la production by tumor necrosis factor-a*
The purpose of this investigation was to determine whether subpopulations of murine lung fibroblasts produced interleukin 1 (IL 1). We previously identified two major populations of pulmonary fibroblasts based on the presence or absence of Thy-1. Thy-l+ and Thy-l-subsets synsthesize fibronectin and type I and I11 collagen, but only the Thy-l-population displays class I1 major histocompatibility complex antigens after stimulation with interferon -y and presents antigen to T helper clones. Interestingly, in the current study we determined that only Thy-l-fibroblast lines and clones synthesized IL 1. Although constitutive production was low, tumor necrosis factor -a (TNF-a) stimulated 5-20-fold increases in IL 1 production inThy-1-fibroblasts. The Thy-l+ fibroblasts did not produce IL 1 even after TNF-a treatment. Northern blot analysis of TNF-a treated cells revealed that in the Thy-l-subset increased mRNA levels for IL la were detected, while IL 1p mRNA was not detected. Furthermore, IL 1 activity from TNF-a-treated Thy-l-fibroblast membranes and supernatants was completely neutralized by IL la-specific antibodies. These observations support the hypothesis that the antigen-presenting Thy-l-subset is important for promoting the inflammation associated with pulmonary fibrosis. In addition, the existence of functional subsets of lung fibroblasts is further substantiated by differential expression of IL 1.
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