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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.
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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.
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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.
Brief Definitive Report
Elisabeth Wieduwild, Mathilde J. Girard-Madoux, Linda Quatrini, Caroline Laprie, Lionel Chasson, Rafaëlle Rossignol, Claire Bernat, Sophie Guia, Sophie Ugolini
Stress hormones increase host susceptibility to viral infection. β2-adrenergic signals in nonhematopoietic cells downmodulate the proinflammatory antiviral natural killer cell response, which is necessary for efficient pathogen elimination. This modulation increases the severity of tissue lesions, decreasing resistance to infection.
Brief Definitive Report
Genki Okumura, Akiko Iguchi-Manaka, Rikito Murata, Yumi Yamashita-Kanemaru, Akira Shibuya, Kazuko Shibuya
This report demonstrated that soluble CD155 interferes with the DNAM-1–mediated antitumor immunity mediated by NK cells and promotes lung colonization of B16/BL6 melanoma cells.
Brief Definitive Report
Roberto R. Ricardo-Gonzalez, Christoph Schneider, Chang Liao, Jinwoo Lee, Hong-Erh Liang, Richard M. Locksley
Activated ILC2s can enter circulation after migratory helminth infection. Using fate-mapping, alarmin-specific knockouts, and methods to isolate tissue-specific perturbations, the authors demonstrate that ILC2 extrusion from tissues reflects activation of pathways specific to receptors on the resident ILC2 population.

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