Lymphokine/monokine inhibition of fibroblast proliferation and collagen production: role in progressive systemic sclerosis (PSS).
Lymphokine/monokine inhibition of fibroblast proliferation and collagen production: role in progressive systemic sclerosis (PSS).
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淋巴因子/单因子抑制成纤维细胞增殖和胶原蛋白生成：在进行性系统性硬化症（PSS）中的作用。
DOI：
10.1111/1523-1747.ep12264686
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Fleischmajer,R
中科院分区：
文献类型：
--
作者：
Duncan,MR;Perlish,JS;Fleischmajer,R
对炎症刺激的正常纤维化反应似乎依赖于激活的单核细胞（MNL）平衡产生许多刺激和抑制成纤维细胞调节介质。为了研究介质生成的改变是否有助于进行性系统性硬化症（PSS）中观察到的纤维化，我们用豆豆蛋白A （Con A）和脂多糖（LPS）刺激人外周血MNL产生大分子介质，抑制培养的正常人成纤维细胞的增殖和胶原生成。这两种Con - a诱导的介质是淋巴因子（LK），因为它们完全由活化的T细胞产生，它们从分子量为50,000的Sephacryl S-200柱中析出。相比之下，两种lps诱导的介质是单因子（MK），因为它们完全由活化的单核细胞产生，并且它们在Mr20,000范围内析出。每对抑制LK和MK也可能是不同的，因为在增殖静止的培养中仍然发生胶原蛋白产生的抑制。对正常志愿者和长期PSS患者产生的成纤维细胞抑制LK/MK水平的定量比较显示，尽管PSS MNL产生正常水平的胶原生成抑制介质，但它们是两种增殖抑制介质的异常产生者。是LK的低生成（-49%）和MK的高生成（+ 196%）。这些结果表明，增殖抑制性LK的产生减少可能允许刺激介质诱导早期活性PSS中观察到的不受限制的成纤维细胞增殖，然后可能通过增殖抑制性MK的产生增加来稳定长期PSS。
A normal fibrotic response to inflammatory stimuli appears to be dependent on the balanced production of a number of stimulatory and inhibitory fibroblast-regulatory mediators by activated mononuclear cells (MNL). To investigate whether altered mediator production contributes to the fibrosis observed in progressive systemic sclerosis (PSS), we stimulated human peripheral blood MNL with concanavalin A (Con A) and lipopolysaccharide (LPS) to produce macromolecular mediators that inhibit the proliferation and the collagen production of cultured normal human fibroblasts. The two Con A-induced mediators were lymphokines (LK) as they were exclusively produced by activated T cells and they coeluted from a Sephacryl S-200 column with a Mrof 50,000. In contrast, the two LPS-induced mediators were monokines (MK) as they were exclusively produced by activated monocytes, and they coeluted in the Mr20,000 range. Each pair of inhibition LK and MK may also be distinct as inhibitions of collagen production still occurred in proliferatively quiescent cultures. A quantitative comparison of the levels of fibroblast-inhibitory LK/MK produced by normal volunteers and long-term PSS patients revealed that although PSS MNL produced normal levels of both collagen production inhibitory mediators, they were aberrant producers of both proliferation inhibitory mediators, being hypo-producers (-49%) of the LK and hyperproducers (+ 196%) of the MK. These results suggest that reduced production of proliferation inhibitory LK may allow stimulatory mediators to induce the unrestricted fibroblast proliferation observed in early active PSS, which then may be stabilized in long-term PSS by the increased production of proliferation inhibitory MK.
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影响因子：
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作者：
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影响因子：
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DOI：
10.1016/0002-9343(62)90241-3
发表时间：
1962
期刊：
The American journal of medicine
影响因子：
--
作者：
L. Hoskins;H. T. Norris;L. Gottlieb;N. Zamcheck
通讯作者：
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