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Cynthia Louis, Cynthia Louis, Fernando Guimaraes, Yuyan Yang, Damian D’Silva, Tobias Kratina, Laura Dagley, Soroor Hediyeh-Zadeh, Jai Rautela, Seth Lucian Masters, Melissa J. Davis, Jeffrey J. Babon, Bogoljub Ciric, Eric Vivier, Warren S. Alexander, Nicholas D. Huntington, Ian P. Wicks
In the present study, Louis et al. identify an inflammatory cascade mediated by IL-18 and GM-CSF–producing NK cells that promotes autoantibody-driven arthritis. GM-CSF signaling in myeloid cells is subsequently restrained by the suppressor of cytokine signaling protein CIS to prevent aberrant GM-CSF–mediated inflammation.
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Michelle A. Francisco, Siyi Wanggou, Jerry J. Fan, Weifan Dong, Xin Chen, Ali Momin, Namal Abeysundara, Hyun-Kee Min, Jade Chan, Rochelle McAdam, Marian Sia, Ronwell J. Pusong, Shixuan Liu, Nish Patel, Vijay Ramaswamy, Noriyuki Kijima, Lu-Yang Wang, Yuanquan Song, Ran Kafri, Michael D. Taylor, Xuejun Li, Xi Huang
Francisco et al. show that chloride intracellular channel 1 (CLIC1) is an evolutionarily conserved regulator of brain tumor growth in Drosophila and medulloblastoma mouse models. CLIC1 cooperates with potassium channels to regulate cell volume homeostasis and rapid cycling of the tumor cells.
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Jeroen F.J. Bogie, Jeroen F.J. Bogie, Elien Grajchen, Elien Wouters, Aida Garcia Corrales, Tess Dierckx, Sam Vanherle, Jo Mailleux, Pascal Gervois, Esther Wolfs, Jonas Dehairs, Jana Van Broeckhoven, Andrew P. Bowman, Ivo Lambrichts, Jan-Åke Gustafsson, Alan T. Remaley, Monique Mulder, Johannes V. Swinnen, Mansour Haidar, Shane R. Ellis, James M. Ntambi, Noam Zelcer, Jerome J.A. Hendriks
In this study, Bogie, Grajchen et al. show that monounsaturated fatty acids formed by stearoyl-CoA desaturase-1 impair the reparative features of macrophages and microglia in demyelinating disorders by reducing their lipid efflux capacity.
Brief Definitive Report
Conor Gruber, Marta Martin-Fernandez, Fatima Ailal, Xueer Qiu, Justin Taft, Jennie Altman, Jérémie Rosain, Sofija Buta, Aziz Bousfiha, Jean-Laurent Casanova, Jacinta Bustamante, Dusan Bogunovic
Gruber et al. describe a gain-of-function mutation in STAT2 that leads to a lethal autoinflammatory disease with autosomal recessive inheritance. This syndrome defines a novel form of type I interferonopathy characterized by impaired regulation of the type I IFN response.
Article
Maria Inês Cunha, Minhui Su, Ludovico Cantuti-Castelvetri, Stephan A. Müller, Martina Schifferer, Minou Djannatian, Ioannis Alexopoulos, Franziska van der Meer, Anne Winkler, Tjakko J. van Ham, Bettina Schmid, Stefan F. Lichtenthaler, Christine Stadelmann, Mikael Simons
We find that pro-inflammatory activation is required for remyelination after myelin injury. We impaired inflammatory signaling and found that microglia in lesioned animals were defective in phagosome maturation, debris clearance, and also in triggering the generation of new oligodendrocytes, a process which required TNF-α.
Article
Yana Zhang, Yajun Wang, Beixue Gao, Yueqi Sun, Liang Cao, Samantha M. Genardi, Chyung-Ru Wang, HuaBin Li, Zhaolin Sun, Yanjie Yang, Deyu Fang
This study identifies USP22 as an essential regulator specifically for iNKT but not conventional T cell development. USP22 suppresses histone H2A monoubiquitination through its interaction with MED1 to partially control expression of genes required for iNKT cell development and differentiation.
Brief Definitive Report
Carlos Diaz-Salazar, Regina Bou-Puerto, Adriana M. Mujal, Colleen M. Lau, Madlaina von Hoesslin, Dietmar Zehn, Joseph C. Sun
Natural killer (NK) cells are critical for protection against viruses. Diaz-Salazar et al. show that adrenergic neurons modulate the adaptive NK cell response in a cell-intrinsic manner. This study identifies the nervous system as a novel axis through which antigen-specific NK cell responses are regulated.

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Volume 217,
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February 3, 2020
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Anne O’Garra, Yasmine Belkaid, Arlene Sharpe, Susan Kaech, Sara Cherry, Emmanuelle Passegué
Academic Editors at JEM share their experiences of being women in STEM and suggest future directions to support the career of female scientists.
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JEM Editorial Team
The editors at JEM share their views on gender bias in scientific publishing and their efforts to ensure that JEM remains a bias-free environment for all authors, reviewers, and editors.

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