The Journal of Experimental Medicine publishes immunology, cancer, stem cells, microbial pathogenesis, vascular biology, and neurobiology research.
The Journal of Experimental Medicine (JEM) features peer-reviewed research on immunology, cancer biology, stem cell biology, microbial pathogenesis, vascular biology, and neurobiology. All editorial decisions are made by research-active scientists in conjunction with in-house scientific editors. JEM provides free online access to many article types immediately, with complete archival content freel
y available online. Established in 1896, JEM is published by The Rockefeller University Press. For more information, visit http://jem.rupress.org. Follow us on Twitter: https://twitter.com/JExpMed Since its inception in 1896, the goal of The Journal of Experimental Medicine (JEM) has been to publish outstanding and enduring studies in medical biology. At a time when many leading publishing groups are establishing topic-specific journals, we believe it is critical to complement that approach by offering a distinguished venue for publication of studies that integrate disciplines within the field of pathogenesis. A distinctive editorial system supports this goal with an emphasis on exceptional service to our authors. Two groups of editors work hand-in hand: professional editors with strong scientific backgrounds, and full-time practicing scientists. At least one editor from each group evaluates the merits of each paper prior to external review. The editors convene weekly to discuss all papers with external referee comments, and reach rapid decisions without excessive requests for revision. Within the field of medical biology we focus both on human studies and diverse in vivo experimental models of human disease that address such topics as genetics, inflammation, immunity, infectious disease, cancer, vascular biology, metabolic disorders, neuroscience, and stem cell biology. We welcome reports ranging from atomic-level analyses to clinical interventions that illustrate new mechanisms.
New Viewpoint: Daniela Salvemini and Timothy Doyle (Saint Louis University) discuss the opportunity to target pro-inflammatory neuro-immune cell interactions in the treatment of neuropathic pain.
Daniela Salvemini and Timothy Doyle discuss the opportunity to target pro-inflammatory neuro-immune cell interactions in the treatment of neuropathic pain.
Ji-Hak Jeong, Shangwei Zhong, Jun-Li Luo (Scripps Research) and colleagues unveil that OBP2A from prostate cancer (PCa) in remission during androgen deprivation therapy enhances PCa growth and myeloid-derived suppressor cell infiltration through interaction with CXCL15/IL8, leading to castration-resistant PCa emergence. Targeting OBP2A of tumor in remission would be effective therapeutic strategy for advanced PCa.
This study unveils that OBP2A from PCa in remission during ADT enhances PCa growth and MDSCs infiltration through interaction with CXCL15/IL8, leading to CRPC e
Researchers at Memorial Sloan Kettering Cancer Center (MSKCC) in New York have discovered that common cancer treatments, such as radiotherapy or anthracycline drugs, cause long-term damage to heart tissue by activating a key inflammatory signaling pathway. The study, published today in the Journal of Experimental Medicine (JEM), suggests that inhibiting this pathway could reduce the chances of cancer survivors suffering heart disease later in life.
Original study: https://bit.ly/3Wt4L5L
Press release:
Researchers at Memorial Sloan Kettering Cancer Center (MSKCC) in New York have discovered that common cancer treatments, such as radiotherapy or anthracycline drugs, cause long-term damage to heart tissue by activating a key inflammatory signaling pathway. The study, published December 19 in the Jou...
Achraf Shamseddine, Suchit H. Patel, Adam M. Schmitt (Memorial Sloan Kettering Cancer Center) and colleagues show that DNA-damaging cancer therapies induce delayed activation of cGAS–STING-dependent type I interferon signaling in the heart. DNA damage–induced cGAS–STING signaling drives cardiac inflammation and late pathologic remodeling of the heart, progressive cardiac functional impairment, and late lethal cardiac toxicity.
🎥 See video summary by Suchit Patel: https://youtu.be/5aW4iEaCNdo
DNA-damaging cancer therapies induce delayed activation of cGAS–STING-dependent type I interferon signaling in the heart. DNA damage–induced cGAS–STING signalin
During influenza virus infection, Treg cell–derived amphiregulin is sensed by EGFR+Collagen-14+ lung mesenchymal cells, stimulating their activation and survival and supporting their role as signaling relay intermediates to promote effective alveolar regeneration. A new study from Katherine A. Kaiser, Nicholas Arpaia and colleagues (Columbia University):
During influenza virus infection, Treg cell–derived amphiregulin is sensed by EGFR+Collagen-14+ lung mesenchymal cells, stimulating their activation and surviva
Jaeu Yi and Chyi-Song Hsieh (Washington University in St. Louis) discuss work from Tanaka et al. (https://bit.ly/3FiEod5) that advances our understanding of how genetic mutants that decrease T cell recognition of antigen, a critical event for immune activation to invading microbes and virus, paradoxically results in autoimmunity.
In this issue of JEM, Tanaka et al. advance our understanding of how genetic mutants that decrease T cell recognition of antigen, a critical event for immune ac
New Spotlight: In the mouse, γδIL17 cells are poised to make IL-17, and these cells have been involved in various infection and cancer models. Edwards et al. (https://bit.ly/3UCg7mH) now report how different γδIL17 subsets are controlled during homeostasis and cancer. From Guillem Sanchez Sanchez and David Vermijlen (ULB - Université libre de Bruxelles):
In the mouse, γδIL17 cells are poised to make IL-17, and these cells have been involved in various infection and cancer models. Edwards et al. now report how di
Qiaoyun Chu, Jing An, Binghui Li and colleagues (Capital Medical University, Beijing) identify a clinical drug, nortriptyline, that can potently inhibit macropinocytosis-mediated fatty acid uptake, and further find that nortriptyline effectively suppresses tumor growth, lipogenesis, and hepatic steatosis in combination with ND-646, a selective ACC1/2 inhibitor.
Chu et al. identify a clinical drug, nortriptyline that can potently inhibit macropinocytosis-mediated fatty acid uptake, and further find that nortriptyline ef
Using epigenomics, transcriptomics, and functional studies, Rafael Han, Ilia Vainchtein, Anna Molofsky and colleagues (UCSF) define mechanisms through which interleukin-33 (IL-33) promotes microglial synapse engulfment during brain development and restricts seizure susceptibility, in part via the induction of pattern recognition receptors including the scavenger receptor MARCO.
Using epigenomics, transcriptomics, and functional studies, we define mechanisms through which interleukin-33 (IL-33) promotes microglial synapse engulfment dur
Lévy, Gothe, Hauck, Béziat (Inserm) and colleagues show that Inherited CARMIL2 deficiency underlies infections, EBV+ smooth muscle tumors, and mucocutaneous inflammation. CARMIL2 deficiency impairs CD28 signaling only partially in T cells but a comparison of CARMIL2 and CD28 deficiency in humans suggests that CARMIL2 governs immunological pathways beyond CD28.
Inherited CARMIL2 deficiency underlies infections, EBV+ smooth muscle tumors, and mucocutaneous inflammation. CARMIL2 deficiency impairs CD28 signaling only par
Takuya Koike, Tomohiro Kurosaki, Wataru Ise et al. (Osaka University) employ a time-stamping method for plasma cells and measure the decay of homeostatic plasma cells with distinct isotypes, or antigen-specific plasma cells that are generated in germinal center–independent or –dependent pathways.
Koike et al. employ a time-stamping method for plasma cells and measure the decay of the homeostatic plasma cells with distinct isotypes, or antigen-specific pl
The underlying mechanisms that drive Th1 responses in the intestine remain unclear. Here, Fatemeh Ahmadi, William Agace and colleagues (Lund University) show that the microbiota-dependent post-weaning accumulation of Th1 cells in the intestine is dependent on cDC1 expression of MHC-II and IL-27.
The underlying mechanisms that drive Th1 responses in the intestine remain unclear. Here, Ahmadi and coworkers show that the microbiota-dependent post-weaning a
We're pleased to present our annual Best of JEM series to highlight cutting-edge research in immunology, host-pathogen interactions, cancer biology, tumor immunology, cardiovascular biology, neuroscience and other areas published in 2022 at JEM. The top 10 papers are selected by the editorial team based, in part, on the number of requests for PDF and full-text HTML versions of an article in the first three months after publication. These studies represent the breadth of JEM’s scope and our longstanding interest in original findings in disease pathogenesis and therapy.
We would also like use this opportunity to thank our authors, reviewers and readers for your interest and continued support for JEM.
We hope you will enjoy this collection and encourage your feedback!
Many aspects of our life and research have changed drastically over the last three years. Nevertheless, the goal of publishing groundbreaking studies at the Journal of Experimental Medicine (JEM) to broaden human knowledge in disease pathogenesis and tr...
Takeshi Inoue, Tomohiro Kurosaki (Osaka University) and colleagues show that antibody feedback plays a role in generating Omicron-reactive memory B cells in SARS-CoV-2 mRNA vaccinees.
Inoue et al. show that the antibody feedback plays a role in generating Omicron-reactive memory B cells in SARS-CoV-2 mRNA vaccinees.
Sarah C. Edwards, Seth B. Coffelt (Cancer Research UK) and colleagues provide deep phenotypic analysis of mouse γδ T cells. They focus functional studies on IL-17A–producing γδ T cell subsets, showing that the co-inhibitory molecules, PD-1 and TIM-3, regulate cell expansion in tumor-bearing mice, which counteracts anti–PD-1 or anti–TIM-3 immunotherapy.
Coffelt, Edwards, and colleagues provide deep phenotypic analysis of mouse γδ T cells. They focus functional studies on IL-17A–producing γδ T cell subsets, show
Postmortem microstructural studies together with in vivo magnetic resonance imaging show that human arachnoid granulations are porous channels that serve as transient filtration conduits for cerebrospinal fluid to flow directly into dural interstitial tissue, but not into venous sinuses.
New Insights from Jean-Leon Thomas (Institut du Cerveau - Paris Brain Institute) & Helene Benveniste discussing work from Shah et al. (https://bit.ly/3FpkP2T):
Postmortem microstructural studies together with in vivo magnetic resonance imaging show that human arachnoid granulations are porous channels that serve as tra
Arachnoid granulations are poorly investigated. This new study by Trishna Shah, Rupal I. Mehta and colleagues (Rush University System for Health) shows that they harbor immune cells and communicate with perisinus spaces, suggesting novel roles in neuroimmunity and glymphatic-lymphatic coupling.
🎥 See video summary by Mehta: https://youtu.be/8jjAJ0612kM
Arachnoid granulations are poorly investigated. We show that they harbor immune cells and communicate with perisinus spaces, suggesting that granulations subser
On the cover of our December Issue: Zhang et al. demonstrate that GABA regulates intestinal stem cell apoptosis through its A receptor in chemoradiotherapy-induced intestinal injury (https://bit.ly/3VmGTR5). The cover shows immunohistochemistry staining for the expression of GABRA1 in the small intestine of human. The image has been modified by the JEM editorial office.
Read JEM’s December Issue: https://bit.ly/3ASZ7ld
How an anomaly in a TCR signaling molecule leads to spontaneous autoimmunity over immunodeficiency is unclear. Atsushi Tanaka, Shinji Maeda, Shimon Sakaguchi (Osaka University) and colleagues show that qualitative/quantitative reduction of ZAP-70 to a critical range produces autoimmune T cells and impairs Treg function, together eliciting autoimmune arthritis and colitis in mice.
How an anomaly in a TCR signaling molecule leads to spontaneous autoimmunity over immunodeficiency is unclear. Qualitative/quantitative reduction of ZAP-70 to a
The study from Pritchard, Phan, Hunter et al. (University of Pennsylvania) identifies a unique role for early T-bet expression in promoting the proliferation of antigen-specific CD8+ T cells following vaccination. Early T-bet expression is necessary for optimal LFA1 expression for appropriate cellular interactions and enables optimal expansion and differentiation of effector and memory CD8+ T cells.
The study identifies a unique role for early T-bet expression in promoting the proliferation of antigen-specific CD8+ T cells following vaccination. Early T-bet
Corinne M. Nielsen, Xuetao Zhang, Rong A. Wang and colleagues (UCSF) show that well-established, Notch4-induced brain arteriovenous malformations are normalized, following deletion of the Notch signaling mediator, Rbpj. Upon complete regression, there are virtually no AVM relapses in adults, even when the causal factor is reintroduced.
Nielsen and Zhang et al. show that well-established, Notch4-induced brain arteriovenous malformations are normalized, following deletion of the Notch signaling
New Insights: Charles R. Schutt and Sho Yamasaki (Osaka University) discuss work from Matute et al. (https://bit.ly/3gs0qAx) finding that a stress-induced lectin, intelectin-1, recruits pathogenic bacteria to the gut and exacerbates colitis.
ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin
ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin the inner mucus layer, and increases colitis severity. ITLN1 upregulation in ulcerative colitis may drive similar outcomes. A new study from Juan D. Matute, Jinzhi Duan, Magdalena B. Flak, Jerrold R. Turner, Richard S. Blumberg (Brigham and Women's Hospital) and colleagues:
ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin
Gillian Carling, Wenjie Luo, and Li Gan (Weill Cornell Medicine) discuss study from Jain et al. (https://bit.ly/3eiuFcd) finding that chronic TREM2 activation by AL002a antibody exacerbates the seeding and spread of pathological tau, enhances the disease-associated microglial signature, and increases neurite dystrophy in 5xFAD mice seeded with Alzheimer’s disease tau.
In this important study, Jain et al. find that chronic TREM2 activation by AL002a antibody exacerbates the seeding and spread of pathological tau, enhances the
“Our group recently used the manuscript transfer process for a paper that had been previously reviewed at a peer journal,” says Mark Anderson of the University of California, San Francisco. “Within days our paper was sent to JEM, and we heard back in less than 10 days about our manuscript and our rebuttal to the previous reviews. A JEM editor provided us with favorable feedback on improving the paper, there was no need for additional experiments, and the paper was swiftly published. We were extremely satisfied with the entire process and believe that this system worked the way it was designed in limiting unneeded rounds of additional review and assessment. We would highly recommend this transfer option to other authors."
When it’s time to move forward during your publication journey, consider JEM. Authors who transfer their papers to JEM appreciate timely initial decisions and clear feedback. Transferred manuscripts are four times more likely to be invited for revisions, and final decisions on transfers that have been previously reviewed are made within 20 days: https://bit.ly/3u4WCc5
To transfer your paper for consideration by JEM editors, simply follow these steps.
Researchers at University of Siena in Italy report on a new mechanism of immune evasion by SARS-CoV-2 based on direct disabling CTLs to form immune synapses through Spike protein binding to ACE2. The authors include Anna Onnis, Emanuele Andreano, Chiara Cassioli, Francesca Finetti, Chiara Della Bella, Oskar Staufer, Elisa Pantano, Valentina Abbiento, Giuseppe Marotta, Mario Milco D’Elios, Rino Rappuoli, and Cosima T. Baldari. According to the study, the mechanism could contribute to the failure of the immune system to control SARS-CoV-2 infection. https://bit.ly/3EyMiP6
See video summary of the study by Onnis: https://youtu.be/Kv0AdZSQj5I
We report a new mechanism of immune evasion by SARS-CoV-2 based on direct disabling CTLs to form immune synapses through Spike protein binding to ACE2. This mec
Andrew Sandstrom (UT Southwestern Medical Center) discusses work from Jenster et al. (https://bit.ly/3zvaf6S) which investigates how UVB radiation promotes activation of the inflammatory immune sensor NLRP1, and in doing so uncover how NLRP1 recognizes a diverse range of ribotoxic stresses.
In this issue of JEM, Jenster et al. investigate how UVB radiation promotes activation of the inflammatory immune sensor NLRP1, and in doing so uncover how NLRP
Akiko Nakayama, Stefan Offermanns (Max Planck Society) and colleagues identify a tumor-suppressing angiocrine function of CCL2 which is inhibited by tumor-derived adrenomedullin acting via its receptor on endothelial cells. Disinhibition of endothelial CCL2 results in reduced tumor progression through inhibition of adrenomedullin formation by tumor cells.
The authors identify a tumor-suppressing angiocrine function of CCL2 which is inhibited by tumor-derived adrenomedullin acting via its receptor on endothelial c
Yifan Zhou, Stephanie S. Watowich (MD Anderson Cancer Center) and colleagues establish murine models of anti-CTLA-4–mediated intestinal irAEs. These reveal common immune signatures and the importance of f***l microbiome dysbiosis as irAE-driving mechanisms, which enable preclinical therapeutic interventions. Key immune features are validated in a cohort of melanoma patients with ICB-associated intestinal irAEs.
Zhou et al. establish murine models of anti-CTLA-4–mediated intestinal irAEs. These reveal common immune signatures and the importance of f***l microbiome dysbi
Our 5th activity with MSK CME is NOW available! �📄 Course content: “Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration” from Zhou et al. (https://bit.ly/3GcPDoe)
What’s a Journal-Based CME activity? A full-text article that is free to read, a multiple-choice question test, and an evaluation/self-assessment. CME course at Memorial Sloan Kettering Cancer Center is available now:
MSK CME, Journal-Based CME: Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration, 11/8/2022 10:00:00 AM - 11/8/2025 11:00:00 PM, This Journal-Based CME activity consists of a full-text article that is free to read, a multiple-choice question test, and an evaluation/self-...
We're pleased to present a special collection to accompany Neuroscience 2022 The collection includes articles on neuro-immune crosstalk, gut-brain axis, neural circuitry in appetite suppression, meningeal lymphatics and meningeal immunity, brain development, memory impairments in Alzheimer's disease, molecular mechanisms underlying Alzheimer's disease, the role of microglia and astrocytes in neural homeostasis and neuropathology, and spinal cord injury. We hope you enjoy this selection and we welcome your feedback!
This collection highlights the latest discoveries in neuroscience, including articles on neuro-immune crosstalk, gut-brain axis, neural circuitry in appetite suppression, meningeal lymphatics and meningeal immunity, brain development, memory impairments...
Integrins mediate the localization of innate-like B cells to the marginal zone of the spleen. By analyzing mice with β1-integrin deficiency in mature B cells, Virginia Andreani, Rudolf Grosschedl and colleagues (Max Planck Institute of Immunobiology and Epigenetics) show that β1-integrin is also required for normal differentiation and function of marginal zone B cells.
Integrins mediate the localization of innate-like B cells to the marginal zone of the spleen. By analyzing mice with β1-integrin deficiency in mature B cells, A
Using systemic EC–pericyte crosstalk analysis, Hao He, Wu Yang, Nan Su, Junhao Hu and colleagues (Shanghai Institute of Organic Chemistry) reveal that nitric oxide–soluble guanylate cyclase signaling mediates endothelial cell–pericyte communication in the lung vasculature and demonstrate that pharmacological activation of the NO–sGC signaling promotes vascular integrity and mitigates inflammation-induced lung injury.
Using systemic EC–pericyte crosstalk analysis, this study identifies the NO–sGC as a key signaling that mediates EC–pericyte communication in the lung vasculatu
Loss of the dNTPase and DNA repair enzyme SAMHD1 is associated with cancer and causes systemic autoimmunity. Tina Schumann, Rayk Behrendt (Rheinische Friedrich-Wilhelms-Universität Bonn) and colleagues show transformation-promoting spontaneous DNA damage and MDA5-driven, but cGAS/STING-dependent, chronic type I interferon production in SAMHD1-deficient mice.
🎥 See video summary of the study by Rayk Behrendt: https://youtu.be/35rVZDwm86w
Loss of the dNTPase and DNA repair enzyme SAMHD1 is associated with cancer and causes systemic autoimmunity. We show transformation-promoting spontaneous DNA da
When you publish with JEM, you can reach more of your community by submitting a short video! We encourage authors of accepted manuscripts to submit video summaries.
SUBSCRIBE 🔔 to our YouTube channel and watch newly posted videos 🎥 https://bit.ly/3SaqRHR
Intact B cell responses to SARS-CoV-2 mRNA vaccines in patients with genetic or acquired type I IFN deficiencies suggest that type I IFNs induced by mRNA vaccines are not required for vaccine efficacy. From Aurélien Sokal, Paul Bastard, Jean-Laurent Casanova, Matthieu Mahévas (Institut Necker Enfants Malades - INEM) and colleagues:
Intact B cell responses to SARS-CoV-2 mRNA vaccines in patients with genetic or acquired type I IFN deficiencies suggest that type I IFNs induced by mRNA vaccin
Our November cover shows a confocal immunofluorescence image of a mouse intestine section after irradiation. Intestinal epithelial cells are marked by GFP (green), and regenerative areas after intestinal damage are labeled with BrdU (red). Blue staining corresponds to cell nuclei (DAPI).
Chaves-Pérez et al. describe an unexpected role of transit-amplifying cells in controlling intestinal stem cell proliferation and organ regeneration (https://bit.ly/3U5kOX0).
Read JEM’s November Issue: https://bit.ly/3NyAJKD
950 3rd Avenue, Fl 2nd
New York, NY
10022
The Journal of Experimental Medicine (JEM) features peer-reviewed research on immunology, cancer biology, stem cell biology, microbial pathogenesis, vascular biology, and neurobiology. All editorial decisions are made by research-active scientists in conjunction with in-house scientific editors. JEM provides free online access to many article types from the date of publication and to all archival content. Established in 1896, JEM is published by The Rockefeller University Press. For more information, visit http://jem.rupress.org. Follow us on Twitter: https://twitter.com/JExpMed
JEM App for iPhone and iPad: https://itunes.apple.com/us/app/journal-experimental-medicine/id481771946
Be the first to know and let us send you an email when Journal of Experimental Medicine posts news and promotions. Your email address will not be used for any other purpose, and you can unsubscribe at any time.
Send a message to Journal of Experimental Medicine:
Today on #InternationalWomensDay we celebrate women scientists #WomenInSTEM who continue to #BreakTheBias! Happy #IWD2022 #WHM2022 https://www.internationalwomensday.com
3D reconstruction of a liver segment showing the distribution of neutrophils (Mrp14+, green) in the tissue, stained for blood vessels (CD31, blue). Cells that are tdTomato positive (red) are derived from the parabiont Ly6GTOM partner mice. Images were acquired with light-sheet microscopy. Video © Casanova-Acebes et al. 2018 in JEM https://bit.ly/2y8Yof7
High-resolution three-dimensional reconstruction of liver vasculature demonstrating bona fide integration of fluorescent-labeled elongated endothelial cells into the endothelial layer. Endothelial cells in the video are represented in gray; GFP+ cells in green. Video © Singhal et al. 2018 in JEM https://bit.ly/2OzUy8e
Live imaging of tumor-associated macrophage subsets (green and cyan) in a mouse lung tumor. Video from Loyher et al. 2018 in JEM https://bit.ly/2CKEtbd
Intravital imaging of mouse proB and preB cells (shown in green). CXCL12-producing cells are shown in red. While proB cells were predominantly static and in direct contact with CXCL12+ cells, with a few proB cells migrating short distances, nearly all preB cells were motile. Video © Fistonich et al. 2018 in JEM http://bit.ly/2NwhxNL
This video shows spontaneously active astrocytes in the hippocampus of an APPPS1 Alzheimer's disease model mouse. Astrocytes were transfected with adeno-associated virus encoding the fluorescent calcium indicator GCaMP6f under the astrocytic GfaABC1D promoter. Video from Reichenbach et al. in JEM http://bit.ly/2rjlR9m
Serial reconstruction of a myelinated fiber from a wild-type mouse sciatic nerve from 350 successive scanning electron microscopy images. Video © Ackerman et al. 2018 in JEM http://bit.ly/2rUwzH5
T follicular helper cells and B cells congregate at the border between the B and T zones of a popliteal lymph node in response to immunization. DsRed+ OT-II T cells are red, CFP+ ICAM-1/2+/+ B1-8hi B cells are blue, and ICAM-1/2−/− CFSE-labeled B1-8hi B cells are green. Video © Zaretsky et al. 2017 in JEM: http://bit.ly/2ls3cIJ
Time-lapse confocal imaging in the ventral wall of caudal aorta of a zebrafish embryo expressing photoactivatable fluorescent protein Dendra2 shows a photoconverted endothelial cell (red) that undergoes endothelial-hematopoietic transition to form a nascent hematopoietic progenitor, which subsequently divides into two daughter cells and migrate to the caudal vein plexus niche. Video © Tian et al. 2017 in JEM http://bit.ly/2lhIbAy
Time lapse video microscopy of hematopoietic stem and progenitor cell "cuddling" by endothelial cells in the caudal hematopoietic tissue of a developing Runx1:mCherry;kdrl:GFP zebrafish embryo. Cuddling is a process in which hematopoietic stem cells adhere to the luminal surface of the sinusoidal endothelial cells, transmigrate to the extraluminal space and there they interact intimately with components of the niche including endothelial cells, stromal cells, and possibly other cells. Video © Blaser et al. 2017 in JEM: http://jem.rupress.org/content/early/2017/03/27/jem.20161616
Recruitment of neutrophils (green) to injury area in the liver (red) after focal hepatic necrosis in vivo. Visualized via spinning disk IVM with a 5×/0.25 FLUAR objective for up to 4 h after focal injury. The video is shown at 42 frames per second. Video © Boras et al. 2017 in JEM http://jem.rupress.org/content/early/2017/02/08/jem.20160647
3D rending of SIM stacks of an OT-II cell/dendritic cell couple show fascin-1 (green) accumulation at the site of OT-II cell/dendritic cell contacts. Actin is shown in red and the nucleus is blue. Video © Chen et al. 2017 in JEM: http://jem.rupress.org/content/early/2017/01/11/jem.20160620
CD4+CD25− T conventional cells (red) or CD4+CD25+ T conventional cells (green) interacting with dendritic cells (cyan) in the lymph node of a mouse. Video © Yan et al. 2017 in JEM: http://jem.rupress.org/content/early/2017/01/11/jem.20160629
When inflammasomes trigger pyroptosis, the plasma membrane tears release soluble cytosolic contents but retains organelles and intracellular bacteria. Neutrophils then efferocytose the pyroptotic cell debris and kill the entrapped bacteria. The video shows the soluble GFP protein released during pyroptosis. Learn more in the new study "Pyroptosis triggers pore-induced intracellular traps (PITs) that capture bacteria and lead to their clearance by efferocytosis" by Ine Jorgensen, Yue Zhang, Bryan A. Krantz, and Edward A. Miao of the Department of Microbiology and Immunology, University of North Carolina at Chapel Hill. http://jem.rupress.org/content/early/2016/08/23/jem.20151613.abstract
Colonize and be counted: Ziętara et al on number of thymus-seeding progenitor niches http://ow.ly/S2AEa
Kitamura et al reveal how a chemokine cascade promotes breast cancer metastasis to the lung. http://ow.ly/Of5OE This time-lapse video shows that Ccr1-deficient macrophages (red) are more frequently detached from cancer cells and move about (see wild-type macrophages interact with cancer cells at http://ow.ly/Of6oc).
Blazek et al (University of Oxford) show that treatment with IFN-λ2/IL-28A halts and reverses the development of collagen-induced arthritis by restricting the recruitment of inflammatory neutrophils. In this video, neutrophils from control mice travel normal distances; you can check out more videos to see how neutrophil migration is impaired in mice treated with IL-28A: http://ow.ly/MyuIL
In My Book® Bookmark/Greeting cards
On The Internet