{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T22:36:11Z","timestamp":1787870171869,"version":"build-2784847793"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"4","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,1,22]]},"abstract":"<jats:p>\n                    CD8 T-cell responses are critical for protection against intracellular pathogens and tumors. The induction and properties of these responses are governed by a series of integrated processes that rely heavily on cell\u2013cell interactions. Intercellular adhesion molecule (ICAM)-1 functions to enhance the strength of antigenic stimulation, extend the duration of contact with antigen-presenting cells, and augment cytokine signals, which are all factors that influence peripheral CD8 T-cell differentiation. Although previous studies suggest that ICAM-1 is essential for establishing memory T-cell populations following peptide immunization, the roles of ICAM-1 in antiviral cellular immunity are less well understood. Here we show that, following a prototypic acute viral infection, the formation and maintenance of memory-phenotype CD127\n                    <jats:sup>hi<\/jats:sup>\n                    , KLRG-1\n                    <jats:sup>lo<\/jats:sup>\n                    CD8 T cells does not require ICAM-1. Nevertheless, ICAM-1 expression on nonlymphocytes dictates the phenotypic and functional attributes of the antiviral CD8 T-cell populations that develop and promotes the gradual attrition of residual effector-like CD127\n                    <jats:sup>lo<\/jats:sup>\n                    , KLRG-1\n                    <jats:sup>hi<\/jats:sup>\n                    CD8 T cells during the memory phase of the response. Although memory T cells do emerge and are maintained if ICAM-1 expression is abolished, the secondary proliferative capacity of these T cells is severely curtailed. Collectively, these studies reveal potential dual roles for ICAM-1 in both promoting the decay of effector responses and programming the sensitivity of memory CD8 T cells to secondary stimuli.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1213480110","type":"journal-article","created":{"date-parts":[[2013,1,8]],"date-time":"2013-01-08T11:50:39Z","timestamp":1357645839000},"page":"1416-1421","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":45,"title":["ICAM-1\u2013dependent tuning of memory CD8 T-cell responses following acute infection"],"prefix":"10.1073","volume":"110","author":[{"given":"Maureen A.","family":"Cox","sequence":"first","affiliation":[{"name":"Departments of aMicrobiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott R.","family":"Barnum","sequence":"additional","affiliation":[{"name":"Departments of aMicrobiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel C.","family":"Bullard","sequence":"additional","affiliation":[{"name":"Genetics, University of Alabama, Birmingham, AL 35294"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allan J.","family":"Zajac","sequence":"additional","affiliation":[{"name":"Departments of aMicrobiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,1,7]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2011.01.004"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.coi.2004.02.005"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2007.12.016"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1139393"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)80376-3"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1521-4141(199901)29:01<45::AID-IMMU45>3.0.CO;2-I"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.165.11.6091"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2008.05.017"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1006\/cimm.2000.1639"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2009.11.010"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2009.11.012"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.4.2201"},{"key":"e_1_3_3_13_2","doi-asserted-by":"crossref","first-page":"6080","DOI":"10.4049\/jimmunol.154.11.6080","article-title":"Novel isoforms of murine intercellular adhesion molecule-1 generated by alternative RNA splicing","volume":"154","author":"King PD","year":"1995","unstructured":"PD King, et al., Novel isoforms of murine intercellular adhesion molecule-1 generated by alternative RNA splicing. 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