{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T15:47:36Z","timestamp":1778600856474,"version":"3.51.4"},"reference-count":36,"publisher":"Proceedings of the National Academy of Sciences","issue":"28","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,7,10]]},"abstract":"<jats:p>\n                    During many acute viral and bacterial infections, IL-7 receptor \u03b1-chain (IL-7R\u03b1) is expressed on a subset of effector CD8 T cells that preferentially develop into long-lived memory CD8 T cells. These cells functionally require IL-7R\u03b1, but it is unclear whether IL-7R\u03b1 acts mainly to induce their differentiation into memory cells or to sustain their long-term survival. To examine this question, IL-7R\u03b1 was constitutively overexpressed on all antigen-specific effector CD8 T cells during viral infection. Constitutive IL-7R\u03b1 expression had minimal effects on the numbers or function of effector and memory CD8 T cells formed. This indicated that IL-7R\u03b1 expression is not sufficient to drive memory cell development. In particular, the forced IL-7R\u03b1 expression did not rescue the killer cell lectin-like receptor G1 (KLRG1)\n                    <jats:sup>hi<\/jats:sup>\n                    short-lived effector CD8 T cells from death, showing that the majority of effector CD8 T cells die in an IL-7R\u03b1-independent manner. Moreover, we found that, regardless of the ectopic expression of IL-7R\u03b1, the KLRG1\n                    <jats:sup>hi<\/jats:sup>\n                    , but not the KLRG1\n                    <jats:sup>lo<\/jats:sup>\n                    effector CD8 T cells, were unable to proliferate well to IL-7, which may be due to increased amounts of p27\n                    <jats:sup>kip<\/jats:sup>\n                    in KLRG1\n                    <jats:sup>hi<\/jats:sup>\n                    cells. Because IL-7 can destabilize p27\n                    <jats:sup>kip<\/jats:sup>\n                    , this result suggested that KLRG1\n                    <jats:sup>hi<\/jats:sup>\n                    and KLRG1\n                    <jats:sup>lo<\/jats:sup>\n                    effector CD8 T cells naturally differ in their ability to transmit IL-7 signals. Altogether, these results reveal that IL-7R\u03b1 expression is permissive, but not instructive, to the creation of memory CD8 T cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0705007104","type":"journal-article","created":{"date-parts":[[2007,7,3]],"date-time":"2007-07-03T20:54:44Z","timestamp":1183496084000},"page":"11730-11735","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":154,"title":["Expression of IL-7 receptor \u03b1 is necessary but not sufficient for the formation of memory CD8 T cells during viral infection"],"prefix":"10.1073","volume":"104","author":[{"given":"Timothy W.","family":"Hand","sequence":"first","affiliation":[{"name":"*Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michel","family":"Morre","sequence":"additional","affiliation":[{"name":"Cytheris, Inc., 92130 Issy-les-Moulineaux, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan M.","family":"Kaech","sequence":"additional","affiliation":[{"name":"*Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; 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