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<jats:title>Skin Reaction</jats:title> <jats:p> Lymphocytes in the skin known as γδ T cells provide an important barrier against infection and injury. Unlike classical αβ T cells, less is known about the molecular requirements of γδ T cell activation. Two studies demonstrate that the junctional adhesion molecule–like protein (JAML) is a costimulatory molecule for mouse γδ T. <jats:bold> Witherden <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1205" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1192698">1205</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5996" page="1154" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1195337">Shaw and Huang</jats:related-article> </jats:bold> ) showed that JAML, binding to its ligand Coxsackie and adenovirus receptor (CAR), leads to proliferation, as well as cytokine and growth factor production by γδ T cells. In vivo, JAML-CAR interactions contributed to the wound healing response in mice. <jats:bold> Verdino <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1210" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1187996">1210</jats:related-article> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5996" page="1154" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1195337"> <jats:bold>Shaw and Huang</jats:bold> </jats:related-article> ) present a crystal structure of CAR/JAML, which revealed an intracellular signaling motif similar to that known for the αβ T cell costimulatory receptor that signals through phosphoinositide 3-kinase. </jats:p>

<jats:title>Skin Reaction</jats:title> <jats:p> Lymphocytes in the skin known as γδ T cells provide an important barrier against infection and injury. Unlike classical αβ T cells, less is known about the molecular requirements of γδ T cell activation. Two studies demonstrate that the junctional adhesion molecule–like protein (JAML) is a costimulatory molecule for mouse γδ T. <jats:bold> Witherden <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1205" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1192698">1205</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5996" page="1154" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1195337">Shaw and Huang</jats:related-article> </jats:bold> ) showed that JAML, binding to its ligand Coxsackie and adenovirus receptor (CAR), leads to proliferation, as well as cytokine and growth factor production by γδ T cells. In vivo, JAML-CAR interactions contributed to the wound healing response in mice. <jats:bold> Verdino <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1210" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1187996">1210</jats:related-article> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5996" page="1154" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1195337"> <jats:bold>Shaw and Huang</jats:bold> </jats:related-article> ) present a crystal structure of CAR/JAML, which revealed an intracellular signaling motif similar to that known for the αβ T cell costimulatory receptor that signals through phosphoinositide 3-kinase. </jats:p>

<jats:title>Gee-Up, NEDD8</jats:title> <jats:p> Diverse bacterial pathogens, such as <jats:italic>Burkholderia pseudomallei</jats:italic> and enteropathogenic <jats:italic>Escherichia coli</jats:italic> (EPEC), inject effector proteins into eukaryotic host cells to subvert host cell biology. <jats:bold> Cui <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1215" related-article-type="in-this-issue" vol="329" xlink:href="10.1126/science.1193844">1215</jats:related-article> ; published online 5 August) show that certain bacterial effector proteins promoted the glutamine deamidation of ubiquitin and the ubiquitin-related protein, NEDD8. The modification of ubiquitin inhibited the formation of polyubiquitin chains while, unexpectedly, the same chemical alteration on NEDD8 interfered with the cell cycle, offering insights not only into the cytopathic effects of bacterial infection but also into mechanisms that may operate during viral infection and cancer. </jats:p>

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