{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T03:32:04Z","timestamp":1752550324845},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,12,12]],"date-time":"2006-12-12T00:00:00Z","timestamp":1165881600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hypergammaglobulinemia and production of autoantibodies occur during many viral infections, and studies have suggested that viral antigen\u2010presenting B cells may become polyclonally activated by CD4 T cells <jats:italic>in vivo<\/jats:italic> in the absence of viral engagement of the BCR. However, we have reported that CD4 cells in lymphocytic choriomengitis virus (LCMV)\u2010infected mice kill adoptively transferred B cells coated with LCMV class II peptides. We report here that most of the surviving na\u00efve B cells presenting class II MHC peptides undergo an extensive differentiation process involving both proliferation and secretion of antibodies. Both events require CD4 cells and CD40\/CD40L interactions but not MyD88\u2010dependent signaling within the B cells. B cells taken from immunologically tolerant donor LCMV\u2010carrier mice with high LCMV antigen load became activated following adoptive transfer into LCMV\u2010infected hosts, suggesting that B cells present sufficient antigen for this process during a viral infection. No division or activation of B cells was detected at all in virus\u2010infected hosts in the absence of cognate CD4 T cells and class II antigen. This approach, therefore, formally demonstrates and quantifies a virus\u2010induced polyclonal proliferation and differentiation of B cells, which, due to their high proportion, would mostly have BCR not specific for the virus.<\/jats:p>","DOI":"10.1002\/eji.200636516","type":"journal-article","created":{"date-parts":[[2006,12,12]],"date-time":"2006-12-12T18:34:37Z","timestamp":1165948477000},"page":"119-128","source":"Crossref","is-referenced-by-count":15,"title":["Dynamics and magnitude of virus\u2010induced polyclonal B cell activation mediated by BCR\u2010independent presentation of viral antigen"],"prefix":"10.1002","volume":"37","author":[{"given":"Evan\u2004R.","family":"Jellison","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Heath\u2004M.","family":"Guay","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eva","family":"Szomolanyi\u2010Tsuda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raymond\u2004M.","family":"Welsh","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,12,21]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830160720"},{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01651349"},{"key":"e_1_2_7_3_2","doi-asserted-by":"crossref","first-page":"3720","DOI":"10.4049\/jimmunol.138.11.3720","article-title":"Infection with the human immunodeficiency virus (HIV) is associated with an in vivo increase in B lymphocyte activation and immaturity.","volume":"138","author":"Martinez\u2010Maza O.","year":"1987","journal-title":"J. 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