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<jats:title>How the thymus shaped immunology</jats:title> <jats:p>The function of the thymus was discovered by Jacques Miller in 1961 and laid a foundation for immunology and modern medicine. Until that time, researchers mistakenly believed the thymus merely represented a remnant of defunct lymph tissue, something of an immune cell graveyard. In a Review, Miller recounts the seminal experiments and conceptual thinking that led to uncovering the critical function of the thymus and provides insights that can be learned from those early days. How knowledge of thymus function subsequently spawned the field of T cell biology and the impact it has had on immune cell interactions, vaccination, cancer immunotherapy, and the microbiome are also discussed.</jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aba2429">eaba2429</jats:related-article> </jats:p>

<jats:title>Revealing family differences</jats:title> <jats:p> In response to low blood glucose concentrations, both the glucagon receptor (GCGR)—a family B G protein–coupled receptor (GPCR)—and the β <jats:sub>2</jats:sub> adrenergic receptor (β <jats:sub>2</jats:sub> AR)—a family A GPCR—are activated and act through the cyclic adenosine monophosphate signaling pathway to increase glucose production. The kinetics of the response is different for the two receptors. Based on structural and spectroscopic data, Hilger <jats:italic>et al.</jats:italic> show that the conformation of transmembrane helix 6 in the activated state is a key differentiator (see the Perspective by Lebon). In β <jats:sub>2</jats:sub> AR, the helix moves toward its active conformation when an agonist binds, but in GCGR, both agonist and G protein binding are required. This likely explains why activation of its partner G protein is slower for GCGR than for β <jats:sub>2</jats:sub> AR. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aba3373">eaba3373</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6503" page="507" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc9291">507</jats:related-article> </jats:p>

<jats:p>The first half of 2020 has seen extraordinary accomplishments in science. The international scientific community has described the genomic sequence of the virus that causes coronavirus disease 2019 (COVID-19) and structures of its important proteins, elucidated principal aspects of the immune response, identified neutralizing antibodies that can serve as therapeutics, and developed promising vaccines. There is much more to learn about COVID-19 and its cause, but the achievements so far are remarkable. So why doesn't this progress feel like the triumph that it is?</jats:p>

<jats:p>A roundup of weekly science policy and related news.</jats:p>

<jats:p>China's "Bat Woman" denies responsibility for the pandemic, demands apology from Trump.</jats:p>

<jats:p>Poor countries fear ending up at the end of the queue.</jats:p>