Beschreibung:
<jats:p><jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> is one of the key molecules bridging the activation of specific <jats:styled-content style="fixed-case">T</jats:styled-content> cells and the maturation of professional and nonprofessional antigen‐presenting cells including <jats:styled-content style="fixed-case">B</jats:styled-content> cells. <jats:styled-content style="fixed-case">CD</jats:styled-content>4<jats:sup>+</jats:sup> T cells have been regarded as the major <jats:styled-content style="fixed-case">T</jats:styled-content>‐cell subset that expresses <jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> upon cognate activation; however, we demonstrate here that a putative <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> helper <jats:styled-content style="fixed-case">T</jats:styled-content>‐cell subset expressing <jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> is induced in human and murine <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells in vitro and in mice immunized with antigen‐pulsed dendritic cells. <jats:styled-content style="fixed-case">IL</jats:styled-content>‐12 and <jats:styled-content style="fixed-case">STAT</jats:styled-content>4‐mediated signaling was the major instructive cytokine signal boosting the ability of <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells to express <jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> both in vitro and in vivo. Additionally, <jats:styled-content style="fixed-case">TCR</jats:styled-content> signaling strength modulated <jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> expression in <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells after primary differentiation in vitro as well as in vivo. The induction of <jats:styled-content style="fixed-case">CD</jats:styled-content>40<jats:styled-content style="fixed-case">L</jats:styled-content> in <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells regulated by <jats:styled-content style="fixed-case">IL</jats:styled-content>‐12 and <jats:styled-content style="fixed-case">TCR</jats:styled-content> signaling may enable <jats:styled-content style="fixed-case">CD</jats:styled-content>8<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells to respond autonomously of <jats:styled-content style="fixed-case">CD</jats:styled-content>4<jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">T</jats:styled-content> cells. Thus, we propose that under proinflammatory conditions, a self‐sustaining positive feedback loop could facilitate the efficient priming of <jats:styled-content style="fixed-case">T</jats:styled-content> cells stimulated by high affinity peptide displaying <jats:styled-content style="fixed-case">APC</jats:styled-content>s.</jats:p>