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首页> 外文期刊>Allergy >NKp46+ cells express granulysin in multiple cutaneous adverse drug reactions.
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NKp46+ cells express granulysin in multiple cutaneous adverse drug reactions.

机译：NKp46 +细胞在多种皮肤不良药物反应中表达颗粒溶素。

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BACKGROUND: The spectrum of cutaneous adverse drug reactions (cADRs) ranges from benign presentations to severe life-threatening forms such as toxic epidermal necrolysis (TEN). In TEN, granulysin has been shown to be the key cytotoxic molecule. Still, little is known about the expression of granulysin in other cADRs. As an important source of granulysin, natural killer (NK) cells are of major interest in cADRs. Recently, NKp46 has been identified as the most selective NK-cell marker. However, the role of NKp46(+) cells in cADRs and their contribution to granulysin expression remain to be elucidated. METHODS: Immunohistochemical and immunofluorescence staining of tissue sections from multiple cADRs were quantitatively and qualitatively evaluated. Further, in vivo and in vitro drug-stimulation tests were performed. RESULTS: Granulysin is expressed at different levels in multiple cADRs both by NKp46(+) cells and by CD8(+) T cells. Even in mild forms of cADRs, granulysin can be induced in vivo and in vitro in a drug-specific manner. NKp46(+) cells were found to infiltrate the dermal/epidermal junction particularly in TEN. CONCLUSION: The impressive clinical differences of cADRs may not be uniquely explained by the expression of granulysin. Additional factors such as drug-specific activation and recruitment of NKp46(+) cells to the epidermis may play a role in determining the severity of cADRs. Therefore, unraveling the effects of drugs on NK-cell activation and trafficking may help to better understand the cytotoxic mechanisms behind cADRs.
机译：背景：皮肤不良药物反应（cADR）的范围从良性表现到严重的威胁生命的形式，例如中毒性表皮坏死溶解（TEN）。在TEN中，颗粒溶素已被证明是关键的细胞毒性分子。但是，关于颗粒溶素在其他cADR中的表达知之甚少。作为颗粒溶素的重要来源，自然杀伤（NK）细胞在cADR中引起了人们的极大兴趣。最近，NKp46被鉴定为最具选择性的NK细胞标记。但是，NKp46（+）细胞在cADR中的作用及其对颗粒溶素表达的贡献仍有待阐明。方法：对来自多个cADR的组织切片的免疫组织化学和免疫荧光染色进行定量和定性评估。此外，进行了体内和体外药物刺激试验。结果：NKp46（+）细胞和CD8（+）T细胞均在多个cADR中以不同水平表达颗粒溶素。即使以轻度形式的cADR，也可以以药物特异性方式在体内和体外诱导颗粒溶素。发现NKp46（+）细胞浸润真皮/表皮连接，特别是在TEN中。结论：cADRs令人印象深刻的临床差异可能不能通过颗粒溶素的表达来唯一解释。其他因素，例如药物特异性激活和NKp46（+）细胞向表皮的募集，可能在确定cADR的严重性中起作用。因此，了解药物对NK细胞活化和运输的影响可能有助于更好地了解cADR背后的细胞毒性机制。

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