A role for endogenous transforming growth factor beta 1 in Langerhans cell biology: the skin of transforming growth factor beta 1 null mice is devoid of epidermal Langerhans cells.
A role for endogenous transforming growth factor beta 1 in Langerhans cell biology: the skin of transforming growth factor beta 1 null mice is devoid of epidermal Langerhans cells.
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内源性转化生长因子β1在Langerhans细胞生物学中的作用：转化生长因子β1空小鼠的皮肤没有表皮Langerhans细胞。
DOI：
10.1084/jem.184.6.2417
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发表时间：
1996-12-01
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转化生长因子 β1 (TGF-β1) 调节白细胞和上皮细胞。为了确定 TGF-β1（一种由角质形成细胞和朗格汉斯细胞 (LC) 产生的细胞因子）的多效性是否延伸至表皮白细胞，我们对 TGF-β1 缺失 (TGF-β1 −/−) 小鼠中的 LC（树突状细胞 [DC] 谱系的表皮部分）和树突状表皮 T 细胞 (DETC) 进行了表征。在由 TGF-β1 -/- 小鼠制备的表皮细胞悬浮液或表皮片中未检测到 I-A+ LC，并且表皮细胞悬浮液缺乏同种刺激活性。相比之下，TGF-β1−/− 小鼠中 TCR-γδ+ DETC 的数量和外观均正常，重要的是，DETC 代表表皮中唯一的白细胞。免疫定位研究显示，尽管 gp40+ DC 不存在，但 TGF-β1 −/− 小鼠的淋巴结中存在 CD11c+ DC。用雷帕霉素治疗 TGF-β1 -/− 小鼠消除了特征性炎症消耗综合征并无限期延长了生存期，但并未导致表皮出现 LC。因此，TGF-β1 -/− 小鼠的LC异常并不是皮肤或其他器官炎症的结果，并且这些动物的LC发育不仅仅是延迟。我们得出结论，内源性 TGF-β1 对于正常小鼠 LC 发育或表皮定位至关重要。
Transforming growth factor β1 (TGF-β1) regulates leukocytes and epithelial cells. To determine whether the pleiotropic effects of TGF-β1, a cytokine that is produced by both keratinocytes and Langerhans cells (LC), extend to epidermal leukocytes, we characterized LC (the epidermal contingent of the dendritic cell [DC] lineage) and dendritic epidermal T cells (DETC) in TGF-β1 null (TGF-β1 −/−) mice. I-A+ LC were not detected in epidermal cell suspensions or epidermal sheets prepared from TGF-β1 −/− mice, and epidermal cell suspensions were devoid of allostimulatory activity. In contrast, TCR-γδ+ DETC were normal in number and appearance in TGF-β1 −/− mice and, importantly, DETC represented the only leukocytes in the epidermis. Immunolocalization studies revealed CD11c+ DC in lymph nodes from TGF-β1 −/− mice, although gp40+ DC were absent. Treatment of TGF-β1 −/− mice with rapamycin abrogated the characteristic inflammatory wasting syndrome and prolonged survival indefinitely, but did not result in population of the epidermis with LC. Thus, the LC abnormality in TGF-β1 −/− mice is not a consequence of inflammation in skin or other organs, and LC development is not simply delayed in these animals. We conclude that endogenous TGF-β1 is essential for normal murine LC development or epidermal localization.