作者: N Yawata , K J Selva , Y-C Liu , K P Tan , A W L Lee
DOI: 10.1038/MI.2015.47
关键词: Conjunctiva 、 NK Cell Lectin-Like Receptor Subfamily C 、 Immune system 、 Biology 、 Cell type 、 Natural killer cell 、 Inflammation 、 Immunology 、 Chemokine 、 Adenovirus infection
摘要: The most severe form of virus-induced inflammation at the ocular surface is epidemic keratoconjunctivitis (EKC), often caused by group D human adenoviruses (HAdVs). We investigated dynamics and mechanisms changes in natural killer (NK) cell types mucosal situ over course infection. In acute phase infection, mature CD56(dim)NK cells that comprise a major subpopulation normal conjunctiva are replaced CD56(bright)NK recruited to chemokines produced infected epithelium, NKG2A-expressing CD56(dim) CD56(bright) NK become subpopulations inflammation. These attracted however incapable mounting strong antiviral response because upregulation inhibitory ligand leukocyte antigen-E (HLA-E) on epithelium. Furthermore, HAdVs downregulate ligands for activating receptors, thus rendering even NKG2A(-)NK unresponsive, an immune-escape mechanism distinct from other adenoviruses. Our findings imply EKC-causing utilize these multiple pathways inhibit responses initial stages