基于免疫的藥物反應(yīng),，如“阿巴卡韋超敏反應(yīng)綜合征”（AHS）和“卡馬西平”-誘導(dǎo)的“Steven Johnson綜合征”（SJS）,，已被與特定的“人白細(xì)胞抗原”（HLA）等位基因聯(lián)系起來(lái)。
刊登在Nature上的文章中,，作者介紹了一個(gè)機(jī)制,，這些小分子藥物通過(guò)該機(jī)制影響抗原呈現(xiàn)，進(jìn)而影響T-細(xì)胞反應(yīng),。通過(guò)以非共價(jià)方式與HLA-B*57：01的“抗原結(jié)合縫”相結(jié)合,，“阿巴卡韋”誘導(dǎo)這個(gè)點(diǎn)的形狀和化學(xué)性質(zhì)發(fā)生變化，因而改變內(nèi)生肽對(duì)HLA的親和性,。
最終,，這將導(dǎo)致表現(xiàn)為AHS的系統(tǒng)性反應(yīng)。研究人員發(fā)現(xiàn),，“卡馬西平”也能與異形HLA-B*15：02結(jié)合,、誘導(dǎo)一個(gè)類(lèi)似的反應(yīng)，這說(shuō)明該機(jī)制具有普遍性,。（生物谷Bioon.com）
doi:10.1038/nature11147
PMC:
PMID:
Immune self-reactivity triggered by drug-modified HLA-peptide repertoire
Patricia T. Illing, Julian P. Vivian, Nadine L. Dudek, Lyudmila Kostenko, Zhenjun Chen, Mandvi Bharadwaj, John J. Miles, Lars Kjer-Nielsen, Stephanie Gras, Nicholas A. Williamson, Scott R. Burrows, Anthony W. Purcell, Jamie Rossjohn & James McCluskey
Human leukocyte antigens (HLAs) are highly polymorphic proteins that initiate immunity by presenting pathogen-derived peptides to T cells1. HLA polymorphisms mostly map to the antigen-binding cleft, thereby diversifying the repertoire of self-derived and pathogen-derived peptide antigens selected by different HLA allotypes2. A growing number of immunologically based drug reactions, including abacavir…
