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1.
PAPER CURRENT
Have Cytokines, Will Travel (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Audrey Baeyens, Susan R. Schwab In many contexts, innate lymphoid cells (ILCs) are primarily tissue resident. By contrast, in a recent issue of Science , Huang et al. (2018) show that inflammatory type 2 ILCs migrate from the intestine to the lungs and that this movement is guided by sphingosine-1-phosphate receptors. Teaser In many contexts, innate lymphoid cells (ILCs) are primarily tissue resident. By contrast, in a recent issue of Science , Huang et al. (2018) show that inflammatory type 2 ILCs migrate from the intestines to the lungs and that this movement is guided by sphingosine-1-phosphate receptors.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
2.
PAPER CURRENT
B Cell Receptor and CD40 Signaling Are Rewired for Synergistic Induction of the c-Myc Transcription Factor in Germinal Center B Cells (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Wei Luo, Florian Weisel, Mark J. Shlomchik Positive selection of germinal center (GC) B cells is driven by B cell receptor (BCR) affinity and requires help from follicular T helper cells. The transcription factors c-Myc and Foxo1 are critical for GC B cell selection and survival. However, how different affinity-related signaling events control these transcription factors in a manner that links to selection is unknown. Here we showed that GC B cells reprogram CD40 and BCR signaling to transduce via NF-κB and Foxo1, respectively, whereas naive B cells propagate both signals downstream of either receptor. Although either BCR or CD40 ligation induced c-Myc in naive B cells, both signals were required to highly induce c-Myc, a critical mediator of GC B cell survival and cell cycle reentry. Thus, GC B cells rewire their signaling to enhance selection stringency via a requirement for both antigen receptor- and T cell-mediated signals to induce mediators of positive selection. Graphical abstract Teaser Luo et al. show that CD40 and BCR signaling in GC B cells is rewired to control very different pathways, and both signals are required for optimal induction of c-Myc, suggesting a mechanism of signaling-directed positive selection of GC B cells.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
3.
PAPER CURRENT
E3 Ligase VHL Promotes Group 2 Innate Lymphoid Cell Maturation and Function via Glycolysis Inhibition and Induction of Interleukin-33 Receptor (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Qian Li, Dulei Li, Xian Zhang, Qingqing Wan, Wen Zhang, Mingke Zheng, Le Zou, Chris Elly, Jee H. Lee, Yun-Cai Liu Group 2 innate lymphoid cells (ILC2s) are a specialized subset of lymphoid effector cells that are critically involved in allergic responses; however, the mechanisms of their regulation remain unclear. We report that conditional deletion of the E3 ubiquitin ligase VHL in innate lymphoid progenitors minimally affected early-stage bone marrow ILC2s but caused a selective and intrinsic decrease in mature ILC2 numbers in peripheral non-lymphoid tissues, resulting in reduced type 2 immune responses. VHL deficiency caused the accumulation of hypoxia-inducible factor 1α (HIF1α) and attenuated interleukin-33 (IL-33) receptor ST2 expression, which was rectified by HIF1α ablation or inhibition. HIF1α-driven expression of the glycolytic enzyme pyruvate kinase M2 downmodulated ST2 expression via epigenetic modification and inhibited IL-33-induced ILC2 development. Our study indicates that the VHL-HIF-glycolysis axis is essential for the late-stage maturation and function of ILC2s via targeting IL-33-ST2 pathway. Graphical abstract Teaser ILC2s are critically involved in allergic responses, but the mechanisms by which they are regulated remain unclear. Li et al. demonstrate that the VHL-HIF axis is essential for ILC2 maturation and function via inhibition of glycolysis and induction of IL-33 receptor expression. These findings have implications for identifying therapeutic targets for allergic diseases.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
4.
PAPER CURRENT
A Macrophage Colony-Stimulating-Factor-Producing γδ T Cell Subset Prevents Malarial Parasitemic Recurrence (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Murad R. Mamedov, Anja Scholzen, Ramesh V. Nair, Katherine Cumnock, Justin A. Kenkel, Jose Henrique M. Oliveira, Damian L. Trujillo, Naresha Saligrama, Yue Zhang, Florian Rubelt, David S. Schneider, Yueh-hsiu Chien, Robert W. Sauerwein, Mark M. Davis Despite evidence that γδ T cells play an important role during malaria, their precise role remains unclear. During murine malaria induced by Plasmodium chabaudi infection and in human P. falciparum infection, we found that γδ T cells expanded rapidly after resolution of acute parasitemia, in contrast to αβ T cells that expanded at the acute stage and then declined. Single-cell sequencing showed that TRAV15N-1 (Vδ6.3) γδ T cells were clonally expanded in mice and had convergent complementarity-determining region 3 sequences. These γδ T cells expressed specific cytokines, M-CSF, CCL5, CCL3, which are known to act on myeloid cells, indicating that this γδ T cell subset might have distinct functions. Both γδ T cells and M-CSF were necessary for preventing parasitemic recurrence. These findings point to an M-CSF-producing γδ T cell subset that fulfills a specialized protective role in the later stage of malaria infection when αβ T cells have declined. Graphical abstract Teaser γδ T cell frequency increases late during mouse and human malaria. Mamedov et al. show that oligoclonal TRAV15N-1 (Vδ6.3) γδ T cells expand across various tissues and prevent late-stage parasitemic recurrence. These protective γδ T cells exhibit a distinct transcriptional profile that includes abundantly expressed M-CSF, which protects against Plasmodium recurrence.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
5.
PAPER CURRENT
Developmental Analysis of Bone Marrow Neutrophils Reveals Populations Specialized in Expansion, Trafficking, and Effector Functions (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Maximilien Evrard, Immanuel W.H. Kwok, Shu Zhen Chong, Karen W.W. Teng, Etienne Becht, Jinmiao Chen, Je Lin Sieow, Hweixian Leong Penny, Goh Chi Ching, Sapna Devi, José Maria Adrover, Jackson L.Y. Li, Ka Hang Liong, Leonard Tan, Zhiyong Poon, Shihui Foo, Jia Wang Chua, I-Hsin Su, Karl Balabanian, Françoise Bachelerie, Subhra K. Biswas, Anis Larbi, William Y.K. Hwang, Vikas Madan, H. Phillip Koeffler, Siew Cheng Wong, Evan W. Newell, Andrés Hidalgo, Florent Ginhoux, Lai Guan Ng Neutrophils are specialized innate cells that require constant replenishment from proliferative bone marrow (BM) precursors as a result of their short half-life. Although it is established that neutrophils are derived from the granulocyte-macrophage progenitor (GMP), the differentiation pathways from GMP to functional mature neutrophils are poorly defined. Using mass cytometry (CyTOF) and cell-cycle-based analysis, we identified three neutrophil subsets within the BM: a committed proliferative neutrophil precursor (preNeu) which differentiates into non-proliferating immature neutrophils and mature neutrophils. Transcriptomic profiling and functional analysis revealed that preNeu require the C/EBPε transcription factor for their generation from the GMP, and their proliferative program is substituted by a gain of migratory and effector function as they mature. preNeus expand under microbial and tumoral stress, and immature neutrophils are recruited to the periphery of tumor-bearing mice. In summary, our study identifies specialized BM granulocytic populations that ensure supply under homeostasis and stress responses. Graphical abstract Teaser The neutrophil differentiation pathway is poorly defined. Evrard et. al. demonstrate a workflow of characterizing bone marrow neutrophil subsets on the basis of their proliferative capacity and molecular signatures and thereby define the developmental trajectory and functional properties of neutrophils.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
6.
PAPER CURRENT
NKp46 Receptor-Mediated Interferon-γ Production by Natural Killer Cells Increases Fibronectin 1 to Alter Tumor Architecture and Control Metastasis (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 20 February 2018 Source: Immunity, Volume 48, Issue 2 Author(s): Ariella Glasner, Assi Levi, Jonatan Enk, Batya Isaacson, Sergey Viukov, Shari Orlanski, Alon Scope, Tzahi Neuman, Claes D. Enk, Jacob H. Hanna, Veronika Sexl, Stipan Jonjic, Barbara Seliger, Laurence Zitvogel, Ofer Mandelboim
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
7.
PAPER CURRENT
New Job for NK Cells: Architects of the Tumor Microenvironment (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 16 January 2018 Source: Immunity, Volume 48, Issue 1 Author(s): Lydia Dyck, Lydia Lynch NK cells control tumor growth directly through targeted cytotoxic granule release or cytokine secretion and indirectly by orchestrating anti-tumor immune responses. In this issue of Immunity , Glasner et al. (2018) now reveal a new role for NK cells in preventing metastatic spread through controlling tumor architecture. Teaser NK cells control tumor growth directly through targeted cytotoxic granule release or cytokine secretion and indirectly by orchestrating anti-tumor immune responses. In this issue of Immunity , Glasner et al. (2018) now reveal a new role for NK cells in preventing metastatic spread through controlling tumor architecture.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
8.
PAPER CURRENT
HIV Immunogens: Affinity Is Key (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 16 January 2018 Source: Immunity, Volume 48, Issue 1 Author(s): Savit Prabhu, Ian A. Cockburn, Carola G. Vinuesa Generation of broadly neutralizing antibodies is a key aim of HIV vaccine design, but the precursor B cells are rare. Abbott et al. (2018) report that high affinity and avidity immunogens are required to promote maturation of low frequency B cells in germinal centers. Teaser Generation of broadly neutralizing antibodies is a key aim of HIV vaccine design, but the precursor B cells are rare. Abbott et al. (2018) report that high affinity and avidity immunogens are required to promote maturation of low frequency B cells in germinal centers.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
9.
PAPER CURRENT
A Long-Distance Relay-tionship between Tumor and Bone (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 16 January 2018 Source: Immunity, Volume 48, Issue 1 Author(s): Klara Soukup, Johanna A. Joyce Myeloid cells, including neutrophils, are important regulators of tumor growth and metastasis. In Science , Engblom et al. (2017) reveal how lung tumors remotely engage bone-resident cells through a relay mechanism that achieves a sustained supply of tumor-promoting neutrophils. Teaser Myeloid cells, including neutrophils, are important regulators of tumor growth and metastasis. In Science , Engblom et al. (2017) reveal how lung tumors remotely engage bone-resident cells through a relay mechanism that achieves a sustained supply of tumor-promoting neutrophils.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.
10.
PAPER CURRENT
Chanzyme TRPM7 Mediates the Ca2+ Influx Essential for Lipopolysaccharide-Induced Toll-Like Receptor 4 Endocytosis and Macrophage Activation (2018)
Elsevier
Publication Date: 2018-02-23
Description: Publication date: 16 January 2018 Source: Immunity, Volume 48, Issue 1 Author(s): Michael S. Schappe, Kalina Szteyn, Marta E. Stremska, Suresh K. Mendu, Taylor K. Downs, Philip V. Seegren, Michelle A. Mahoney, Sumeet Dixit, Julia K. Krupa, Eric J. Stipes, Jason S. Rogers, Samantha E. Adamson, Norbert Leitinger, Bimal N. Desai Toll-like receptors (TLRs) sense pathogen-associated molecular patterns to activate the production of inflammatory mediators. TLR4 recognizes lipopolysaccharide (LPS) and drives the secretion of inflammatory cytokines, often contributing to sepsis. We report that transient receptor potential melastatin-like 7 (TRPM7), a non-selective but Ca 2+ -conducting ion channel, mediates the cytosolic Ca 2+ elevations essential for LPS-induced macrophage activation. LPS triggered TRPM7-dependent Ca 2+ elevations essential for TLR4 endocytosis and the subsequent activation of the transcription factor IRF3. In a parallel pathway, the Ca 2+ signaling initiated by TRPM7 was also essential for the nuclear translocation of NFκB. Consequently, TRPM7-deficient macrophages exhibited major deficits in the LPS-induced transcriptional programs in that they failed to produce IL-1β and other key pro-inflammatory cytokines. In accord with these defects, mice with myeloid-specific deletion of Trpm7 are protected from LPS-induced peritonitis. Our study highlights the importance of Ca 2+ signaling in macrophage activation and identifies the ion channel TRPM7 as a central component of TLR4 signaling. Graphical abstract Teaser Schappe et al. show that genetic deletion of Trpm7 in macrophages or pharmacological inhibition of TRPM7 channel prevents macrophage activation due to the loss of TRPM7-mediated Ca 2+ influx in response to LPS. The study identifies TRPM7 as a Ca 2+ -entry pathway required for macrophage activation.
Print ISSN: 1074-7613
Electronic ISSN: 1097-4180
Topics: Medicine
Published by Elsevier on behalf of Cell Press.