Echinococcus granulosus is a food-borne zoonotic disease that greatly burdens public health and the economy. It is common in livestock breeding and rural areas. Circulating transmission in nature is caused by intermediate hosts becoming infected by accidentally consuming insect eggs. [1][2][3] Hence, vaccination against circular propagation is essential for controlling E. granulosus infection. 4 Our previous study found that immunization with rEg.P29 resulted in protective efficacy of 94.5% and 96.6% in sheep and mice, respectively, providing powerful evidence for the potential of rEg.P29 as an anti-E. granulosus vaccine. 5 In addition, modern molecular biology

Background Adaptive immune response has been thought to play a key role in SARS-CoV-2 infection. The role of B cells, CD4+T, and CD8+T cells are different in vaccine-induced immune response, thus it is imperative to explore the functions and kinetics of adaptive immune response. We collected blood samples from unvaccinated and vaccinated individuals. To assess the mechanisms contributing to protective immunity of CoronaVac vaccines, we mapped the kinetics and durability of humoral and cellular immune responses after primary and boost vaccination with CoronaVac vaccine in different timepoints. Materials and methods We separate PBMC and plasma from blood samples. The differentiation and function of RBD-spcific CD4+T and CD8+T cells were analyzed by flow cytometry and ELISA. Antibodies response was analyzed by ELISA. ELISPOT analysis was perfomed to detected the RBD-spcific memory B cells. CBA analysis was performed to detected the cytokine immune profiles. Graphpad prism 8 and Origin 2021 were used for statistical analysis. Results Vaccine-induced CD4+T cell responses to RBD were more prominent than CD8+T cell responses, and characterized by a predominant Th1 and weak Th17 helper response. CoronaVac vaccine triggered predominant IgG1 antibody response and effectively recalled specific antibodies to RBD protein after booster vaccination. Robust antigen-specific memory B cells were detected (p < 0.0001) following booster vaccination and maintained at 6 months (p < 0.0001) following primary vaccination. Vaccine-induced CD4+T cells correlated with CD8+T cells (r = 0.7147, 0.3258, p < 0.0001, p = 0.04), memory B cell responses (r = 0.7083, p < 0.0001), and IgG and IgA (r = 0.6168, 0.5519, p = 0.0006, 0.003) after vaccination. In addition, vaccine induced a broader and complex cytokine pattern in plasma at early stage. Conclusion Taken together, these results highlight the potential role of B cell and T cell responses in vaccine-induced long-term immunity.

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Introduction Echinococcus granulosus (E. granulosus) causes a hazardous zoonotic parasitic disease. This parasite can occupy the liver and several areas of the body, causing incurable damage. Our previous studies have provided evidence that the recombinant protein P29 (rEg.P29) exhibit immune protection in sheep and mice against pathological damage induced by E. granulosus, showing its potential as candidate for vaccine development. However, information on the B‐cell epitopes of rEg.P29 has not yet been reported. Methods Immunological model was established in mice with rEg.P29. SDS‐PAGE and Western blot were used to identify protein. Screening for B‐cell dominant epitope peptides of rEg.P29 by enzyme‐linked immunosorbent assay (ELISA) and immune serum. Dominant epitopes were validated using ELISA and flow cytometry. Multiple sequence alignment analysis was performed using BLAST and UniProt. Results Immunization with rEg.P29 induced intense and persistent antibody responses, and the epitope of the dominant antigen of B cells are identified as rEg.P29166–185 (LKNAKTAEQKAKWEAEVRKD). Anti‐rEg.P29166–185‐specific antibodies lack epitopes against IgA, IgE, and IgG3, compared to anti‐rEg.P29‐specific antibodies. However, anti‐rEg.P29166–185 IgG showed comparatively higher titers, as determined among those peptides by endpoint titration. In addition, rEg.P29 and rEg.P29166–185 promote B‐cell activation and proliferation in vitro. The dominant epitopes are relatively conserved in different subtypes of the rEg.P29 sequence. Conclusion rEg.P29166–185 can act as a dominant B‐cell epitope for rEg.P29 and promote cell activation and proliferation in the same way as rEg.P29.