{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T11:05:54Z","timestamp":1767179154285,"version":"build-2238731810"},"update-to":[{"DOI":"10.1371\/journal.ppat.1013345","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2025,7,14]],"date-time":"2025-07-14T00:00:00Z","timestamp":1752451200000}}],"reference-count":56,"publisher":"Public Library of Science (PLoS)","issue":"7","license":[{"start":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T00:00:00Z","timestamp":1752019200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01 AI171408"],"award-info":[{"award-number":["R01 AI171408"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R21 AI154198"],"award-info":[{"award-number":["R21 AI154198"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["T32HL076122"],"award-info":[{"award-number":["T32HL076122"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000024","name":"Canadian Institutes for Health Research","doi-asserted-by":"crossref","award":["PJT-159525"],"award-info":[{"award-number":["PJT-159525"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    The polyclonal, T-dependent nature of hypergammaglobulinemia during murine infection with LCMV is well defined, however the mechanism by which polyclonal B cells acquire antigens for presentation remains unknown. Here we use LCMV-specific CD4\u2009+\u2009transgenic T cells to explore several hypotheses for B cell antigen uptake. We found that antigens produced by cells infected with LCMV\n                    <jats:italic>in vitro<\/jats:italic>\n                    are available to polyclonal B cells and their presentation to CD4+ T cells enabled robust co-activation. The\n                    <jats:italic>in vitro<\/jats:italic>\n                    nature of our model demonstrates that\n                    <jats:italic>in vivo<\/jats:italic>\n                    factors such as cytokine milieu and antigen release by NK\/CD8+ are not required. We show that non-replicative UVC-irradiated LCMV enables antigen access to B cells, thus productive infection of B cells is not required for antigen acquisition. B cells loaded with LCMV antigens\n                    <jats:italic>in vitro<\/jats:italic>\n                    can efficiently present these antigens to CD4+ T cells in LCMV-infected mice, thereby validating our model\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Using transmission electron microscopy we identified LCMV-GP bearing particles of various sizes including &lt;50nm, a size accessible to B cells via pinocytosis. The particles morphologically resemble exosomes or viral particles (infective or defective interfering). We show that polyclonal B cell access to Ag is maintained when exosome release or viral defective interfering particle release is inhibited. Finally, we used a monovalent Fab derived from the LCMV-neutralizing antibody KL25 to show that access to the viral GP1 protein is important in order for polyclonal B cells to efficiently acquire LCMV antigen for presentation, suggesting the presence of a GP1 receptor on B cells.\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1013345","type":"journal-article","created":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T17:51:27Z","timestamp":1752083487000},"page":"e1013345","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Polyclonal B cells acquire LCMV antigens in a GP1-dependent manner"],"prefix":"10.1371","volume":"21","author":[{"given":"Gabriel","family":"Chamberlain","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guillaume L.","family":"Lopez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L\u00e9a","family":"Bourguignon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xavier","family":"Laulh\u00e9","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasmine","family":"Adda-Bouchard","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tania","family":"Charpentier","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rebekah","family":"Honce","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jason W.","family":"Botten","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7913-871X","authenticated-orcid":true,"given":"Alain","family":"Lamarre","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"340","published-online":{"date-parts":[[2025,7,9]]},"reference":[{"issue":"4","key":"ppat.1013345.ref001","doi-asserted-by":"crossref","first-page":"343","DOI":"10.1038\/ni911","article-title":"Hypergammaglobulinemia and autoantibody induction mechanisms in viral infections","volume":"4","author":"L Hunziker","year":"2003","journal-title":"Nat Immunol"},{"issue":"3","key":"ppat.1013345.ref002","first-page":"396","article-title":"LCMV-specific CD4 T cell dependent polyclonal B-cell activation upon persistent viral infection is short lived and extrafollicular. 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