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喹诺酮类光过敏:由全身性给予光半抗原药物引起的光敏性皮炎。

Quinolone photoallergy: photosensitivity dermatitis induced by systemic administration of photohaptenic drugs.

作者信息

Tokura Y

机构信息

Department of Dermatology, Hamamatsu University School of Medicine, Japan.

出版信息

J Dermatol Sci. 1998 Sep;18(1):1-10. doi: 10.1016/s0923-1811(98)00026-7.

Abstract

Quinolone antibacterial agents are well known to elicit photosensitivity as a side effect. The photoallergenicity of fluoroquinolones, the representative quinolone derivatives, is mainly derived from their photohaptenic moiety. When epidermal cells are irradiated with ultraviolet A light in the presence of fluoroquinolones, quinolone photoadducts are formed in the treated cells. This photomodification is thought to be an initial step for sensitization and elicitation of this photoallergy, and quinolone-photoderivatized Langerhans cells are capable of stimulating immune T cells in mice. In the murine model, fluoroquinolone photoallergy is mediated by Th1 cells bearing T cell receptor Vbeta 13. There is a broad photoantigenic cross-reactivity among fluoroquinolones in recognition by T cells and immunoglobulins. Therefore, it is most likely that fluoroquinolones carry the same photoantigenic epitope, which is recognized by Vbetal3+ T cells, leading to fluoroquinolone photosensitivity and cross-reactivity.

摘要

喹诺酮类抗菌剂作为副作用引发光过敏是众所周知的。代表性喹诺酮衍生物氟喹诺酮类的光致敏性主要源于其光半抗原部分。当在氟喹诺酮类存在的情况下用紫外线A照射表皮细胞时,在处理过的细胞中会形成喹诺酮光加合物。这种光修饰被认为是该光过敏致敏和激发的初始步骤,并且喹诺酮光衍生化的朗格汉斯细胞能够刺激小鼠的免疫T细胞。在小鼠模型中,氟喹诺酮光过敏由携带T细胞受体Vβ13的Th1细胞介导。在T细胞和免疫球蛋白的识别中,氟喹诺酮类之间存在广泛的光抗原交叉反应性。因此,氟喹诺酮类很可能携带相同的光抗原表位,该表位被Vβ13 + T细胞识别,导致氟喹诺酮类光过敏和交叉反应性。

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