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It also does not fully restore HIV<\/jats:styled-content>\u2010induced gut damage unless administered extremely early after infection. Additional biomarkers are needed to evaluate the capacity of therapies aimed at HIV<\/jats:styled-content> remission\/cure to restore HIV<\/jats:styled-content>\u2010induced intestinal immune damage and limit chronic inflammation. Herein, we aimed to identify a systemic surrogate marker whose levels would reflect gut immune damage such as intestinal Th17 cell loss starting from primary HIV<\/jats:styled-content>\u20101 infection.<\/jats:p><\/jats:sec>Methods<\/jats:title>Biomarker discovery approaches were performed in four independent cohorts, covering HIV<\/jats:styled-content>\u20101 primary and chronic infection in 496 na\u00efve or cART<\/jats:styled-content>\u2010treated patients (Amsterdam cohort (ACS<\/jats:styled-content>), ANRS PRIMO<\/jats:styled-content>, COPANA<\/jats:styled-content> and CODEX<\/jats:styled-content> cohorts). The concentration and activity of soluble Dipeptidylpeptidase 4 (sDPP<\/jats:styled-content>4) were quantified in the blood from these patients, including pre\u2010 and post\u2010infection samples in the ACS<\/jats:styled-content> cohort. For quantification of DPP<\/jats:styled-content>4 in the gut, we utilized two non\u2010human primate models, representing pathogenic (macaque) and non\u2010pathogenic (African green monkey) SIV<\/jats:styled-content> infection. Four gut compartments were analysed in each animal model (ileum, jejunum, colon and rectum) for quantification of DPP<\/jats:styled-content>4<\/jats:italic>, RORC<\/jats:styled-content><\/jats:italic> and TBX<\/jats:styled-content>21<\/jats:italic> gene expression in sorted CD<\/jats:styled-content>4+<\/jats:sup> cells. To analyse if sDPP<\/jats:styled-content>4 levels increase when Th17 cells were restored, we quantified sDPP<\/jats:styled-content>4 in plasma from SIV<\/jats:styled-content>\u2010infected macaques treated with IL<\/jats:styled-content>\u201021.<\/jats:p><\/jats:sec>Results<\/jats:title>We showed that sDPP<\/jats:styled-content>4 levels were strongly decreased in primary HIV<\/jats:styled-content>\u20101 infection. Strikingly, sDPP<\/jats:styled-content>4 levels in primary HIV<\/jats:styled-content>\u20101 infection predicted time to AIDS<\/jats:styled-content>. They were not increased by cART<\/jats:styled-content> in chronic HIV<\/jats:styled-content>\u20101 infection (median 36\u00a0months on cART<\/jats:styled-content>). In the gut of SIV<\/jats:styled-content>\u2010infected non\u2010human primates, DPP<\/jats:styled-content>4 <\/jats:italic>mRNA<\/jats:styled-content> was higher in CD<\/jats:styled-content>4+<\/jats:sup> than CD<\/jats:styled-content>4\u2212<\/jats:sup> leucocytes. DPP<\/jats:styled-content>4 specifically correlated with RORC<\/jats:styled-content> expression, a Th17 marker, in CD<\/jats:styled-content>4+<\/jats:sup> cells from the intestine. We further demonstrated that sDPP<\/jats:styled-content>4 activity levels were increased in animals treated with IL<\/jats:styled-content>\u201021 and that this increase was associated with restoration of the Th17 compartment and reduced inflammation. Furthermore, DPP<\/jats:styled-content>4 <\/jats:italic>mRNA<\/jats:styled-content> levels in small intestine CD<\/jats:styled-content>4+<\/jats:sup> cells positively correlated with circulating DPP<\/jats:styled-content>4 activity.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>These data provide evidence that blood sDPP<\/jats:styled-content>4 levels could be useful as a correlate for HIV<\/jats:styled-content>\u2010induced intestinal damage.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jia2.25144","type":"journal-article","created":{"date-parts":[[2018,7,10]],"date-time":"2018-07-10T08:48:19Z","timestamp":1531212499000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Systemic DPP<\/scp>4 activity is reduced during primary HIV<\/scp>\u20101 infection and is associated with intestinal RORC<\/scp>+<\/sup>CD<\/scp>4+<\/sup> cell levels: a surrogate marker candidate of HIV<\/scp>\u2010induced intestinal damage"],"prefix":"10.1002","volume":"21","author":[{"given":"Micka\u00ebl J","family":"Ploquin","sequence":"first","affiliation":[{"name":"Institut Pasteur Unit\u00e9 HIV Inflammation et Persistance Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Armanda","family":"Casrouge","sequence":"additional","affiliation":[{"name":"Institut Pasteur Unit\u00e9 Immunobiologie des cellules dendritiques Paris France"},{"name":"INSERM U1223 Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoann","family":"Madec","sequence":"additional","affiliation":[{"name":"Institut Pasteur URE Epid\u00e9miologie des Maladies Emergentes Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4055-617X","authenticated-orcid":false,"given":"Nicolas","family":"No\u00ebl","sequence":"additional","affiliation":[{"name":"Institut Pasteur Unit\u00e9 HIV Inflammation et Persistance Paris 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