Viral blockade of the transporter associated with antigen processing (TAP) diminishes surface and endosomal recycling compartment levels of major histocompatibility complex class-I (MHC-I) in dendritic cells (DCs), and compromises both classical MHC-I presentation and canonical cross-presentation during infection to impair CD8 T-cell immunity. Virus-specific CD8 T cells are thought to be cross-primed mostly by uninfected TAP-sufficient DCs through cross-presentation of viral peptides from internalized virus-infected dying cells. The dilemma is that CD8 T cells primed to TAP-dependent viral peptides are mismatched to the TAP-independent epitopes presented on tissues infected with immune-evasive viruses. Noncanonical cross-presentation in DCs overcomes cell-intrinsic TAP blockade to nevertheless prime protective TAP-independent CD8 T cells best-matched against the infection. Exploitation of noncanonical cross-presentation may prevent chronic infections with immune-evasive viruses. It may also control immune-evasive cancers that have downmodulated TAP expression.

与抗原加工 (TAP) 相关的转运蛋白的病毒阻断会降低树突状细胞 (DC) 中主要组织相容性复合物 I 类 (MHC-I) 的表面和内体回收区室水平，并损害经典的 MHC-I 呈递和典型交叉。感染期间的表现会损害 CD8 T 细胞免疫。病毒特异性 CD8 T 细胞被认为主要是由未感染的 TAP 充足的 DC 通过交叉呈递来自内化病毒感染的死亡细胞的病毒肽来交叉引发的。困境在于，TAP 依赖性病毒肽引发的 CD8 T 细胞与感染免疫逃避病毒的组织上呈现的 TAP 独立表位不匹配。DC 中的非典型交叉呈递克服了细胞固有的 TAP 阻断，从而启动了与感染最匹配的保护性 TAP 独立 CD8 T 细胞。利用非规范交叉表达可以预防免疫逃避病毒的慢性感染。它还可以控制 TAP 表达下调的免疫逃避癌症。