Abstract:
BACKGROUND:While vaccination remains the most effective method to control hepatitis B virus (HBV) infection, 5-10% of recipients exhibit non-responsiveness to the HB vaccine. Immunological analysis of strong, weak or absent protective antibody responses to the HB vaccine should provide insights into the mechanisms that contribute to non-responsiveness. RESULTS:We investigated the potential involvement of follicular helper T (Tfh) cells in the immune response to HB vaccine, and associations between the miR-17-92 cluster and Tfh cells. We recruited 12 adults who had completed the HB vaccination course during childhood. Following a booster dose of HB vaccine, hepatitis B surface antibody (HBsAb) titers, percentage of PD-1+ICOS+ circulating Tfh (cTfh) and plasma cells, and expression of miR-17-92 were assessed at baseline (before immunization) and after vaccination on days 7 and 14. Notably, the HBsAb level gradually increased after HB vaccination while the proportion of PD-1+ICOS+ cTfh cells was significantly increased on day 7 relative to baseline, so as plasma cells. Expression of miR-18a and miR-17 within the miR-17-92 cluster and HBsAb titers in CD4+ T cells were positively correlated with the PD-1+ICOS+ cTfh cells proportions after HB vaccination. CONCLUSIONS:The increase in HBsAb titers was positively associated with expression of all the components of the miR-17-92 cluster except miR-19a. Our findings indicate that the miR-17-92 cluster contributes to antibody production, and miR-18a and miR-17 are involved in Tfh cells differentiation after HB vaccination.
journal_name
BMC Immunoljournal_title
BMC immunologyauthors
Xu X,Li Y,Liang Y,Yin M,Yu Z,Zhang Y,Huang L,Ni Jdoi
10.1186/s12865-018-0263-ysubject
Has Abstractpub_date
2018-07-28 00:00:00pages
25issue
1issn
1471-2172pii
10.1186/s12865-018-0263-yjournal_volume
19pub_type
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