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Delayed drug hypersensitivity reactions - new concepts.

机译：药物超敏反应延迟-新概念。

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Immune reactions to small molecular compounds such as drugs can cause a variety of diseases mainly involving skin, but also liver, kidney, lungs and other organs. In addition to the well-known immediate, IgE-mediated reactions to drugs, many drug-induced hypersensitivity reactions appear delayed. Recent data have shown that in these delayed reactions drug-specific CD4(+) and CD8(+) T cells recognize drugs through their T cell receptors (TCR) in an MHC-dependent way. Immunohistochemical and functional studies of drug-reactive T cells in patients with distinct forms of exanthems revealed that distinct T cell functions lead to different clinical phenotypes. Taken together, these data allow delayed hypersensitivity reactions (type IV) to be further subclassified into T cell reactions, which by releasing certain cytokines and chemokines preferentially activate and recruit monocytes (type IVa), eosinophils (type IVb), or neutrophils (type IVd). Moreover, cytotoxic functions by either CD4(+) or CD8(+) T cells(type IVc) seem to participate in all type IV reactions. Drugs are not only immunogenic because of their chemical reactivity, but also because they may bind in a labile way to available TCRs and possibly MHC-molecules. This seems to be sufficient to stimulate certain, probably preactivated T cells. The drug seems to bind first to the fitting TCR, which already exerts some activation. For full activation, an additional interaction of the TCR with the MHC molecules is needed. The drug binding to the receptor structures is reminiscent of a pharmacological interaction between a drug and its (immune) receptor and was thus termed the p-i concept. In some patients with drug hypersensitivity, such a response occurs within hours even upon the first exposure to the drug. The T cell reaction to the drug might thus not be due to a classical, primary response, but is due to peptide-specific T cells which happen to be stimulated by a drug. This new concept has major implications for understanding clinical and immunologicalfeatures of drug hypersensitivity and a model to explain the frequent skin symptoms in drug hypersensitivity is proposed.
机译：对药物等小分子化合物的免疫反应会引起多种疾病，主要涉及皮肤，但也涉及肝，肾，肺和其他器官。除了众所周知的即时的，IgE介导的药物反应外，许多药物引起的超敏反应似乎也被延迟。最新数据表明，在这些延迟反应中，药物特异性CD4（+）和CD8（+）T细胞通过其T细胞受体（TCR）以MHC依赖性方式识别药物。对不同形式的兴奋剂患者进行药物反应性T细胞的免疫组织化学和功能研究表明，不同的T细胞功能导致不同的临床表型。综上所述，这些数据可以将迟发型超敏反应（IV型）进一步细分为T细胞反应，通过释放某些细胞因子和趋化因子优先激活并募集单核细胞（IVa型），嗜酸性粒细胞（IVb型）或嗜中性粒细胞（IVd型）。 ）。此外，CD4（+）或CD8（+）T细胞（IVc型）的细胞毒性功能似乎参与了所有IV型反应。药物不仅因其化学反应而具有免疫原性，而且还因为它们可能以不稳定的方式与可利用的TCR和可能的MHC分子结合。这似乎足以刺激某些可能预激活的T细胞。该药物似乎首先与合适的TCR结合，而TCR已经发挥了一定的活化作用。为了完全活化，需要TCR与MHC分子的额外相互作用。药物与受体结构的结合使人联想到药物与其（免疫）受体之间的药理相互作用，因此被称为p-i概念。在一些具有药物超敏反应的患者中，即使在首次接触药物后，这种反应也会在数小时内发生。因此，T细胞对药物的反应可能不是由于经典的主要反应，而是由于恰好被药物刺激的肽特异性T细胞所致。该新概念对于理解药物超敏反应的临床和免疫学特征具有重要意义，并提出了一种解释药物超敏反应中常见皮肤症状的模型。

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