{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T20:50:55Z","timestamp":1790369455744,"version":"4.1.0"},"reference-count":80,"publisher":"American Society for Microbiology","issue":"18","license":[{"start":{"date-parts":[[2007,9,15]],"date-time":"2007-09-15T00:00:00Z","timestamp":1189814400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2007,9,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Recent studies have established a protective role for T cells during primary West Nile virus (WNV) infection. Binding of CD40 by CD40 ligand (CD40L) on activated CD4\n            <jats:sup>+<\/jats:sup>\n            T cells provides an important costimulatory signal for immunoglobulin class switching, antibody affinity maturation, and priming of CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell responses. We examined here the function of CD40-dependent interactions in limiting primary WNV infection. Compared to congenic wild-type mice, CD40\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice uniformly succumbed to WNV infection. Although CD40\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice produced low levels of WNV-specific immunoglobulin M (IgM) and IgG, viral clearance from the spleen and serum was not altered, and CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell priming in peripheral lymphoid tissues was normal. Unexpectedly, CD8\n            <jats:sup>+<\/jats:sup>\n            T-cell trafficking to the central nervous system (CNS) was markedly impaired in CD40\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, and this correlated with elevated WNV titers in the CNS and death. In the brains of CD40\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, T cells were retained in the perivascular space and did not migrate into the parenchyma, the predominant site of WNV infection. In contrast, in wild-type mice, T cells trafficked to the site of infection in neurons. Beside its role in maturation of antibody responses, our experiments suggest a novel function of CD40-CD40L interactions: to facilitate T-cell migration across the blood-brain barrier to control WNV infection.\n          <\/jats:p>","DOI":"10.1128\/jvi.00941-07","type":"journal-article","created":{"date-parts":[[2007,7,12]],"date-time":"2007-07-12T00:44:49Z","timestamp":1184201089000},"page":"9801-9811","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":64,"title":["CD40-CD40 Ligand Interactions Promote Trafficking of CD8\n            <sup>+<\/sup>\n            T Cells into the Brain and Protection against West Nile Virus Encephalitis"],"prefix":"10.1128","volume":"81","author":[{"given":"Elizabeth","family":"Sitati","sequence":"first","affiliation":[{"name":"Departments of Molecular Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin E.","family":"McCandless","sequence":"additional","affiliation":[{"name":"Pathology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robyn S.","family":"Klein","sequence":"additional","affiliation":[{"name":"Pathology and Immunology"},{"name":"Medicine"},{"name":"Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Diamond","sequence":"additional","affiliation":[{"name":"Departments of Molecular Microbiology"},{"name":"Pathology and Immunology"},{"name":"Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200102)31:2<527::AID-IMMU527>3.0.CO;2-D"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200324717"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.193.8.967"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/30996"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.183.5.2129"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.72.9.7440-7449.1998"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1072615"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.3.1505"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1473-3099(02)00368-7"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.184.2.747"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.77.4.2578-2586.2003"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20031223"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid0704.017408"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.it.2005.07.004"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.77.24.12941-12949.2003"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3863-05.2006"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2003-04-1244"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1997.8843"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20051970"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1473-3099(04)01128-4"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.273.5283.1864"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1038\/378617a0"},{"key":"e_1_3_2_24_2","unstructured":"Sci. 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