{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:22:24Z","timestamp":1790338944572,"version":"4.1.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2001,5,1]],"date-time":"2001-05-01T00:00:00Z","timestamp":988675200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>T cell deletion and\/or inactivation were considered the leading mechanisms for neonatal tolerance. However, recent investigations have indicated that immunity develops at the neonatal stage but evolves to guide later T cell responses to display defective and\/or biased effector functions. Although neonatal-induced T cell modulation provides a useful approach to suppress autoimmunity, the mechanism underlying the biased function of the T cells remains unclear. In prior studies, we found that exposure of newborn mice to Ig-PLP1, a chimera expressing the encephalitogenic proteolipid protein (PLP) sequence 139\u2013151, induced deviated Th2 lymph node cells producing IL-4 instead of IL-2 and anergic splenic T cells that failed to proliferate or produce IFN-\u03b3 yet secreted significant amounts of IL-2. However, if assisted with IFN-\u03b3 or IL-12, these anergic splenic T cells regained full responsiveness. The consequence of such biased\/defective T cells responses was protection of the mice against experimental allergic encephalomyelitis. In this study, investigations were performed to delineate the mechanism underlying the novel form of IFN-\u03b3-dependent splenic anergy. Our findings indicate that CD40 ligand expression on these splenic T cells is defective, leading to noneffective cooperation between T lymphocytes and APCs and a lack of IL-12 production. More striking, this cellular system revealed a requirement for IL-2R expression for CD40 ligand-initiated, IL-12-driven progression of T cells into IFN-\u03b3 production.<\/jats:p>","DOI":"10.4049\/jimmunol.166.9.5594","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:42:04Z","timestamp":1398022924000},"page":"5594-5603","source":"Crossref","is-referenced-by-count":12,"title":["Neonatal Exposure to Antigen Induces a Defective CD40 Ligand Expression that Undermines Both IL-12 Production by APC and IL-2 Receptor Up-Regulation on Splenic T Cells and Perpetuates IFN-\u03b3-Dependent T Cell Anergy"],"prefix":"10.1093","volume":"166","author":[{"given":"Booki","family":"Min","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin L","family":"Legge","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J Jeremiah","family":"Bell","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Randal K","family":"Gregg","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lequn","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacque C","family":"Caprio","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Habib","family":"Zaghouani","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Tennessee , Knoxville, TN 37996"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2001,5,1]]},"reference":[{"key":"2026020209182037200_R1","first-page":"4217","volume-title":"J. 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