{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:06:07Z","timestamp":1791183967242,"version":"4.1.0"},"reference-count":32,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5270","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1996,6,28]]},"abstract":"<jats:p>\n            T cell proliferation in vivo is presumed to reflect a T cell receptor (TCR)-mediated polyclonal response directed to various environmental antigens. However, the massive proliferation of T cells seen in viral infections is suggestive of a bystander reaction driven by cytokines instead of the TCR. In mice, T cell proliferation in viral infections preferentially affected the CD44\n            <jats:sup>hi<\/jats:sup>\n            subset of CD8\n            <jats:sup>+<\/jats:sup>\n            cells and was mimicked by injection of polyinosinic-polycytidylic acid [poly(I:C)], an inducer of type I interferon (IFN I), and also by purified IFN I; such proliferation was not associated with up-regulation of CD69 or CD25 expression, which implies that TCR signaling was not involved. IFN I [poly(I:C)]-stimulated CD8\n            <jats:sup>+<\/jats:sup>\n            cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8\n            <jats:sup>+<\/jats:sup>\n            cells. IFN I also potentiated the clonal expansion and survival of CD8\n            <jats:sup>+<\/jats:sup>\n            cells responding to specific antigen. Production of IFN I may thus play an important role in the generation and maintenance of specific memory.\n          <\/jats:p>","DOI":"10.1126\/science.272.5270.1947","type":"journal-article","created":{"date-parts":[[2006,10,27]],"date-time":"2006-10-27T18:30:41Z","timestamp":1161973841000},"page":"1947-1950","source":"Crossref","is-referenced-by-count":827,"title":["Induction of Bystander T Cell Proliferation by Viruses and Type I Interferon in Vivo"],"prefix":"10.1126","volume":"272","author":[{"given":"David F.","family":"Tough","sequence":"first","affiliation":[{"name":"D. F. Tough and J. Sprent, Department of Immunology, IMM4, Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Persephone","family":"Borrow","sequence":"additional","affiliation":[{"name":"P. Borrow, Department of Neuropharmacology, IMM6, Scripps Research Institute, 10666 North Torrey Pines Road, La Jolla, California 92037, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Sprent","sequence":"additional","affiliation":[{"name":"D. F. Tough and J. 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