Jem Immunology Collection 2020 Why Submit to Jem?
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JEM IMMUNOLOGY COLLECTION 2020 WHY SUBMIT TO JEM? FORMAT NEUTRAL You may submit your papers in ANY format. 92% OF INVITED REVISIONS ARE ACCEPTED. TRANSFER POLICY We welcome submissions that include reviewer comments from another journal. You may also request manuscript transfer between Rockefeller University Press journals, and we can confidentially send reviewer reports and identities to another journal beyond RUP. INITIAL DECISION IN 6 DAYS FAIR AND FAST We limit rounds of revision, and we strive to provide clear, detailed decisions that illustrate what is expected in the revisions. Articles appear online one to two days after author proofs are returned. TIME IN PEER REVIEW 38 DAYS OPEN ACCESS OPTIONS Our options include Immediate Open Access (CC-BY) and open access six months after publication (CC-BY-NC-SA). *Median 2019 An Editorial Process Guided by Your Community At JEM, all editorial decisions on research manuscripts are made through collaborative consultation between professional scientific editors and the academic editorial board. Submission or transfer Academic and scientific If appropriate, sent Academic and scientific Informed decisions editors review to Peer Review editors review comments sent to authors Revised manuscript Academic and scientific 92% of invited Published online Circulated via alerts and submission and rereview editors review revisions accepted* 1-2 days after author social media to readers proofs returned around the world JEM IMMUNOLOGY COLLECTION 2020 or over 120 years, the Journal of Experimental Medicine (JEM) has been the venue for seminal studies in the field of immunology, spanning from basic concept to F translational science. These discoveries have paved the way for major advances in the field of immunology and in the development of groundbreaking therapeutic approaches. This JEM special collection presents recent and exciting advances in immunology ranging from fundamental concepts to human immunology and interaction of pathogens with the host immune system. We hope you enjoy this collection and encourage your comments on Twitter at @JExpMed. Interested in learning how we are making the publishing process easier for authors? Visit jem.org, or contact the Editorial office at [email protected]. 5 Human IL2RB mutations cause autoimmunity and immunodeficiency Two groups of researchers describe patients with a loss of immunity and peripheral immune tolerance arising from autosomal recessive mutations in the IL2RB gene Isabel Z. Fernandez ... Ross M. Kedl, Cullen M. Dutmer, Elena W.Y. Hsieh. Zinan Zhang … Sophie Hambleton, Caroline Rooryck, Kenneth G.C. Smith, Michael J. Lenardo 7 IL-18BP deficiency causes fulminant viral hepatitis Excessive IL-18 signaling causes the body’s immune system to attack and kill healthy liver cells, leading to catastrophic liver failure in response to hepatitis A infection Serkan Belkaya … Jean-Laurent Casanova 8 A virulence factor in cis and trans The Toxoplasma gondii protein ROP16 suppresses the host immune response by altering the behavior of both infected and uninfected macrophages Longfei Chen, David A. Christian, Josh Kochanowsky ... Anita A. Koshy, Christopher A. Hunter 9 RIPK1 can kill without its kinase activity Simultaneous innate immune priming and TAK1 inactivation by microbial pathogens causes RIPK1 to induce inflammatory cell death and sepsis independently of its kinase activity R.K. Subbarao Malireddi, Prajwal Gurung ... Thirumala-Devi Kanneganti 10 How skin γδ T cells stay positioned Sphingosine-1-phosphate receptor 2 and CD69 cooperate to keep γδ T cells from leaving the dermis Brian J. Laidlaw, Elizabeth E. Gray ... Jason G. Cyster 11 BCOR enhances T helper 17 cell formation BCL6 corepressor works together with KDM2B to generate T cell subset that helps promote clearance of Brochure articles: Ben Short, PhD, extracellular bacteria Christina Szalinski, PhD Jessica A. Kotov ... Micah D. Gearhart, Marc K. Jenkins Design: Christine Candia 12 IL-2 scales the size of the T reg population On the cover: A human tonsil section Self-reactive thymocytes modulate the size of the regulatory T cell population generated in the thymus through analyzed by imaging mass cytometry, using production of IL-2 DNA intercalator staining and merged Saskia Hemmers ... Alexander Y. Rudensky signals from membrane markers to detect individual cells. Image ©2019 Durand et 13 New method to detect “hidden” HIV-1 al. Related source: Durand, M., T. Walter, T. A combination of quadruplex qPCR and next-generation sequencing can detect latent reservoirs of HIV-1 Pirnay, T. Naessens, P. Gueguen, C. Goudot, S. Christian Gaebler ... Michel C. Nussenzweig Lameiras, Q. Chang, N. Talaei, O. Ornatsky, T. Vassilevskaia, S. Baulande, S. Amigorena, E. 14 “Adaptive” natural killer cells correlate with protection from malaria Segura. 2019. Human lymphoid organ cDC2 and macrophages play complementary roles in In people exposed to Plasmodium falciparum, “adaptive” natural killer cells appear to protect against malaria T follicular helper responses. J. Exp. Med. 216: Geoffrey T. Hart … Eric O. Long 1561–1581. https://doi.org/10.1084/jem.20181994 3 Executive Editor Advisory Editors Teodoro Pulvirenti Shizuo Akira Vijay K. Kuchroo Hans Schreiber phone (212) 327-8575 Kari Alitalo Ralf Kuppers Pamela Schwartzberg email: [email protected] Frederick W. Alt Tomohiro Kurosaki Charles N. Serhan Editorial Board Co-Chairs David Artis Bart N. Lambrecht Nilabh Shastri Carl Nathan K. Frank Austen Ross Levine Ethan M. Shevach Michel Nussenzweig Albert Bendelac Klaus F. 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Hunter Rino Rappuoli Andrew McMichael Luisa Iruela-Arispe Jeffrey Ravetch Luigi Notarangelo Akiko Iwasaki Nicholas Restifo Federica Sallusto Jos Jonkers Nikolaus Romani Toshio Suda Johanna Joyce David L. Sacks Thirumala-Devi Kanneganti Shimon Sakaguchi Consulting Biostatistical Gerard Karsenty Matthew D. Scharff Editor Jay Kolls Olaf Schneewind Xi Kathy Zhou Paul Kubes Stephen P. Schoenberger Senior Preflight Editor Production Manager Copyright to articles published in this journal is held by the authors. Articles are published Laura Smith Camille Clowery by Rockefeller University Press under license from the authors. Conditions for reuse of the articles by third parties are listed at http://www.rupress.org/terms Preflight Editor Production Designer Rochelle Ritacco Erinn A. Grady Print ISSN 0022-1007 Online ISSN 1540-9538 Production Editor Jennifer McGullam Rockefeller University Press HUMAN IL2RB MUTATIONS CAUSE AUTOIMMUNITY AND IMMUNODEFICIENCY Two groups of researchers describe patients with a loss of immunity and peripheral immune tolerance arising from autosomal recessive mutations in the IL2RB gene The cytokine interleukin-2 (IL-2) plays a disease in humans. Mutations in IL2RA, key role in helping the immune system encoding the IL-2R α chain, for exam- fight infections while avoiding attacks ple, cause an early-onset autoimmune on the body’s own, healthy tissues. Pri- syndrome, whereas mutations in IL2RG, marily produced by CD4+ helper T cells encoding the γ subunit, cause a severe upon exposure to foreign antigens, IL-2 combined immunodeficiency associat- stimulates the proliferation of both T ed with the loss of both T and NK cells. cells and natural killer (NK) cells to fight Hypomorphic mutations in IL2RG have invading microbes. But IL-2 also sup- also been reported to cause autoim- ports peripheral tolerance by promoting munity and immunodeficiency. But no the development of regulatory T cells defects had ever been reported in the and the clonal deletion of peripheral, gene encoding IL-2Rβ until two groups self-reactive T cells. of researchers independently identified several kindreds with autosomal reces- The high-affinity IL-2 receptor (IL-2R) sive mutations in IL2RB. is a trimeric protein composed of α, Compared with cells