{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T17:49:30Z","timestamp":1791568170310,"version":"4.3.4"},"reference-count":49,"publisher":"National Academy of Sciences","issue":"9","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2002,4,30]]},"abstract":"<jats:p>\n                    We analyzed for the first time the expression of chemokines in subpopulations of the murine immune system at the single-cell level. We demonstrate\n                    <jats:italic>in vitro<\/jats:italic>\n                    and in a model of murine listeriosis that macrophage inflammatory protein (MIP)-1\u03b1, MIP-1\u03b2, regulated on activation normal T cell expressed and secreted (RANTES), and activation-induced, T cell-derived, and chemokine-related cytokine (ATAC)\/lymphotactin are cosecreted to a high degree with IFN-\u03b3 by activated individual natural killer (NK), CD8\n                    <jats:sup>+<\/jats:sup>\n                    T, and CD4\n                    <jats:sup>+<\/jats:sup>\n                    T helper 1 (Th1) cells. Functionally, ATAC and the CC chemokines cooperate with IFN-\u03b3 in the up-regulation of CD40, IL-12, and tumor necrosis factor-\u03b1, molecules playing a central role in the effector phase of macrophages. Our data indicate that (\n                    <jats:italic>i<\/jats:italic>\n                    ) MIP-1\u03b1, MIP-1\u03b2, RANTES, and ATAC are not only chemoattractants but also coactivators of macrophages, (\n                    <jats:italic>ii<\/jats:italic>\n                    ) MIP-1\u03b1, MIP-1\u03b2, RANTES, and ATAC constitute together with IFN-\u03b3 a group of \u201ctype 1 cytokines,\u201d and (\n                    <jats:italic>iii<\/jats:italic>\n                    ) these cytokines act together as a functional unit that is used by NK cells in the innate phase and then \u201chanded over\u201d to CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells in the antigen-specific phase of the immune defense, thus bridging the two components of a Th1 immune reaction.\n                  <\/jats:p>","DOI":"10.1073\/pnas.092141999","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:46:49Z","timestamp":1027680409000},"page":"6181-6186","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":267,"title":["MIP-1\u03b1, MIP-1\u03b2, RANTES, and ATAC\/lymphotactin function together with IFN-\u03b3 as type 1 cytokines"],"prefix":"10.1073","volume":"99","author":[{"given":"Brigitte G.","family":"Dorner","sequence":"first","affiliation":[{"name":"Molecular Immunology, Robert Koch-Institute, D-13353 Berlin, Germany; Deutsches Rheuma-Forschungszentrum, D-10117 Berlin, Germany; Max Planck Institute for Infection Biology, D-10117 Berlin, Germany; and Child Health Research Institute, North Adelaide SA 5006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Scheffold","sequence":"additional","affiliation":[{"name":"Molecular Immunology, Robert Koch-Institute, D-13353 Berlin, Germany; Deutsches Rheuma-Forschungszentrum, D-10117 Berlin, Germany; Max Planck Institute for Infection Biology, D-10117 Berlin, Germany; and Child Health Research Institute, North Adelaide SA 5006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Rolph","sequence":"additional","affiliation":[{"name":"Molecular Immunology, Robert Koch-Institute, D-13353 Berlin, Germany; Deutsches Rheuma-Forschungszentrum, D-10117 Berlin, Germany; Max Planck Institute for Infection Biology, D-10117 Berlin, Germany; and Child Health Research Institute, North Adelaide SA 5006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin B.","family":"H\u00fcser","sequence":"additional","affiliation":[{"name":"Molecular Immunology, Robert Koch-Institute, D-13353 Berlin, Germany; Deutsches Rheuma-Forschungszentrum, D-10117 Berlin, Germany; Max Planck Institute for Infection Biology, D-10117 Berlin, Germany; and Child Health Research Institute, North Adelaide SA 5006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan H. 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