Some research advances of immune mechanism during infection in China

Yang, Wei

In opposition to host protective strategy, some pathogens may be able to evade and subvert immune responses. Programmed death 1 (PD-1), a negative regulator for activation, expansion and acquisition of effector functions of T cells, is well involved in pathogen evasion strategies [33, 34] . Although extensive studies have been performed on function of PD-1, as so far regulation mechanism of PD-1 expression has not been reported. Zheng and colleagues have identified and characterized the promoter and upstream regulation region of mouse PD-1, providing important clues for the PD-1 gene transcriptional regulation [35] . In addition, papain-like proteases (PLPs), produced by coronavirus such as SARS and NL63, attenuate the innate response against virus through their IFN antagonism activities. As deubiquitinating enzymes, PLPs block polyI:C-induced activation of Interferon regulatory factor 3 (IRF3) and NF-κB, thus reducing IFN induction. Meanwhile, PLPs deactivate ERIS, an endoplasmic reticulum IFN stimulator, by inhibiting the ERIS dimerization [36] [37] [38] [39] [40] [41] . Another mechanism involved in pathogen evasion is induced by IbeT, an E. coli K1 pathogenicity island gene. It has been shown that IbeT contributes to escape from the lysosomes into the cytoplasm for replication after E. coli K1 invasion into human brain microvascular endothelial cells [42, 43] .