Kupper T S, McGuire J
J Invest Dermatol. 1986 Nov;87(5):570-3. doi: 10.1111/1523-1747.ep12455811.
Epidermal thymocyte activating factor (ETAF) is spontaneously released into the media by PAM 212 and A 431 cell lines and cultured normal human keratinocytes. ETAF from all 3 cell types can substitute for interleukin 1 (IL-1) in the augmentation of proliferation of a helper T-cell clone (D10.G4.1) induced by mitogen. Hydrocortisone (HC) substantially reduces the release of ETAF by these keratinocytes and, further, appears to induce the release of an inhibitor of lymphocyte activating factor activity of IL-1. Irradiation with UVC causes increased ETAF release into the media. Hydrocortisone abrogates this effect. Thus HC reduces both constitutive and elicited release of ETAF. ETAF plays a major role in inflammation; the ability of HC to block ETAF release by keratinocytes may account for the anti-inflammatory effect of glucocorticosteroids on the skin.
表皮胸腺细胞活化因子（ETAF）可由PAM 212和A 431细胞系以及培养的正常人角质形成细胞自发释放到培养基中。来自所有3种细胞类型的ETAF在增强丝裂原诱导的辅助性T细胞克隆（D10.G4.1）增殖方面可替代白细胞介素1（IL-1）。氢化可的松（HC）可显著减少这些角质形成细胞释放ETAF，此外，似乎还能诱导释放一种抑制IL-1淋巴细胞活化因子活性的物质。用紫外线C（UVC）照射会导致ETAF释放到培养基中的量增加。氢化可的松可消除这种效应。因此，HC可减少ETAF的组成性释放和诱导性释放。ETAF在炎症中起主要作用；HC阻断角质形成细胞释放ETAF的能力可能解释了糖皮质激素对皮肤的抗炎作用。
