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Immunol."],"abstract":"<jats:p>\n                    <jats:italic>Cystic echinococcosis<\/jats:italic>\n                    (CE) is a zoonotic parasitic disease spread worldwide caused by\n                    <jats:italic>Echinococcus granulosus<\/jats:italic>\n                    (\n                    <jats:italic>E<\/jats:italic>\n                    g), which sometimes causes serious damage; however, in many cases, people are not aware that they are infected. A number of recombinant vaccines based on\n                    <jats:italic>E<\/jats:italic>\n                    g are used to evaluate their effectiveness against the infection. Our previous report showed that recombinant\n                    <jats:italic>E<\/jats:italic>\n                    g.P29 (r\n                    <jats:italic>E<\/jats:italic>\n                    g.P29) has a marvelous immunoprotection and can induce Th1 immune response. Furthermore, data of miRNA microarray in mice spleen CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells showed that miR-126a-5p was significantly elevated 1 week after immunization by using r\n                    <jats:italic>E<\/jats:italic>\n                    g.P29. Therefore, in this perspective, we discussed the role of miR-126a-5p in the differentiation of naive CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells into Th1\/Th2 under r\n                    <jats:italic>E<\/jats:italic>\n                    g.P29 immunization and determined the mechanisms associated with delta-like 1 homolog (DLK1) and Notch1 signaling pathway. One week after P29 immunization of mice, we found that miR-126a-5p was significantly increased and DLK1 expression was decreased, while Notch1 pathway activation was enhanced and Th1 response was significantly stronger. The identical conclusion was obtained by overexpression of mmu-miR-126a-5p in primary naive CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells in mice. Intriguingly, mmu-miR-126a-5p was significantly raised in serum from mice infected with protoscolex in the early stages of infection and markedly declined in the late stages of infection, while has-miR-126-5p expression was dramatically reduced in serum from CE patients. Taken together, we show that miR-126a-5p functions as a positive regulator of Notch1-mediated differentiation of CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells into Th1 through downregulating DLK1\n                    <jats:italic>in vivo<\/jats:italic>\n                    and\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Hsa-miR-126-5p is potentially a very promising diagnostic biomarker for CE.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2022.773276","type":"journal-article","created":{"date-parts":[[2022,2,8]],"date-time":"2022-02-08T06:00:25Z","timestamp":1644300025000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["The Recombinant Eg.P29-Mediated miR-126a-5p Promotes the Differentiation of Mouse Naive CD4+ T Cells via DLK1-Mediated Notch1 Signal 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