RESUMO
Previous studies have demonstrated that lipid rafts and ßadducin serve an important role in leukocyte rolling. In the present study the migratory ability and behavior of neutrophils was demonstrated to rely on the integrity of the lipid raft structure. ßadducin was demonstrated to have a critical role in neutrophil migration. Knockdown of ßadducin attenuated the migratory ability of dHL60 cells and the distribution of ßadducin in lipid raft structures was changed by Nformylmethionylleucylphenylalanine treatment. Furthermore, the findings demonstrated that the tyrosine phosphorylation of ßadducin was required for its relocation. The results of the present study suggested that the lipid raftassociated protein ßadducin may be a novel control point for the excessive infiltration of neutrophils during inflammation.
Assuntos
Movimento Celular , Proteínas do Citoesqueleto/metabolismo , Microdomínios da Membrana/metabolismo , Neutrófilos/metabolismo , Adulto , Feminino , Células HL-60 , Humanos , Masculino , N-Formilmetionina Leucil-Fenilalanina/análogos & derivados , N-Formilmetionina Leucil-Fenilalanina/farmacologia , Neutrófilos/citologiaRESUMO
The present study aimed to investigate the distribution of T follicular helper (Tfh)-cell subsets in patients with hepatitis B virus (HBV) and determine the underlying mechanism of HBV regulation of Tfh cells. The frequency of peripheral blood Tfh subsets was analyzed using flow cytometry. The expression level of programmed cell death1 (PD1) and prostaglandin E2 (PGE2) was quantified using reverse transcriptionquantitative polymerase chain reaction and western blotting. The PGE2 level in culture supernatant was detected using enzymelinked immunosorbent assay. A Transwell chamber was used to coculture Tfh cells with HepG2 and HepG2.2.1.5. The percentage of inducible Tcell costimulator (ICOS)+ and total Tfh cells was high at the immune activation (IA) group; however, it was reduced in the immune tolerance (IT), responders with HBsAg seroconversion (RP) and healthy control (HC) groups. The percentage of PD1+ Tfh cells was significantly higher in IA and IT compared with RP and HC. The ratio of PD1+/total Tfh cells was positively correlated with the load of HBV DNA; therefore, this ratio may act as an indicator for HBV replication. The expression level of PD1 in Tfh cells was higher in the HepG2.2.1.5 cocultured group compared with the HepG2 group, this may be due to the high PGE2 expression level in HBVinfected HepG2.2.1.5 cells. The findings of the present study revealed an imbalanced distribution of PD1+ Tfh cells in patients with HBV at different immune phases. Additionally, HBV may upregulate the expression of PD1 in Tfh cells by promoting HepG2.2.1.5 to secret PGE2. Identifying the effect of HBV on Tfhcell subsets is crucial for improving immuno-based therapy for HBV.