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  • 1.
    Bernink, Jochem H.
    et al.
    University of Amsterdam, Netherlands; Royal Netherlands Academic Arts and Science KNAW, Netherlands.
    Mjösberg, Jenny
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Institute, Sweden.
    Spits, Hergen
    University of Amsterdam, Netherlands.
    Letter: Human ILC1: To Be or Not to Be in IMMUNITY, vol 46, issue 5, pp 756-7572017In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 46, no 5, p. 756-757Article in journal (Other academic)
    Abstract [en]

    n/a

  • 2.
    Chen, J.
    et al.
    Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Boston, Massachusetts, USA.
    Stewart, V.
    Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Boston, Massachusetts, USA.
    Spyrou, Giannis
    Department of Biosciences at Novum, Center for Biotechnology, Karolinska Institutet, Huddinge, Sweden.
    Hilberg, F.
    Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Boston, Massachusetts, USA.
    Wagner, E. F.
    Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Boston, Massachusetts, USA.
    Alt, F. W.
    Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Boston, Massachusetts, USA.
    Generation of normal T and B lymphocytes by c-jun deficient embryonic stem cells1994In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 1, no 1, p. 65-72Article in journal (Refereed)
    Abstract [en]

    To determine the potential roles of c-jun in lymphocyte development, we generated somatic chimeric mice by injecting homozygous c-jun mutant embryonic stem (ES) cells into blastocysts from recombination activating gene-2 (RAG-2)-deficient mice. Chimeric mice had poor restoration of thymocytes, but contained substantial numbers of mature T and B lymphocytes in the periphery. Stimulation of c-jun-/- B cells resulted in normal levels of proliferation and immunoglobulin secretion. Likewise, stimulation of c-jun-/- T cells resulted in essentially normal levels of IL-2R alpha expression, IL-2 secretion, and proliferation. We further showed that the relatively normal activation responses of the c-jun-/- T cells probably results from the fact that other members of the Jun family contribute to the bulk of the activator protein-1 (AP-1) complexes in normal T cells and, as a result, AP-1 complexes are found at relatively normal levels in c-jun-/- T cells.

  • 3. Constantin, G
    et al.
    Majeed, Meytham
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology.
    Giagulli, C
    Piccio, L
    Kim, JY
    Butcher, EC
    Laudanna, C
    Chemokines trigger immediate beta2 integrin affinity and mobility changes: Differential regulation and roles in lymphocytes arrest under flow.2000In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 13, p. 759-769Article in journal (Refereed)
  • 4. Dias, Sheila
    et al.
    Månsson, Robert
    Gurbuxani, Sandeep
    Sigvardsson, Mikael
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Experimental Hematology .
    Kee, Barbara L.
    E2A Proteins Promote Development of Lymphoid-Primed Multipotent Progenitors2008In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 29, no 2, p. 217-227Article in journal (Refereed)
    Abstract [en]

    The first lymphoid-restricted progeny of hematopoietic stem cells (HSCs) are lymphoid-primed multipotent progenitors (LMPPs), which have little erythromyeloid potential but retain lymphoid, granulocyte, and macrophage differentiation capacity. Despite recent advances in the identification of LMPPs, the transcription factors essential for their generation remain to be identified. Here, we demonstrated that the E2A transcription factors were required for proper development of LMPPs. Within HSCs and LMPPs, E2A proteins primed expression of a subset of lymphoid-associated genes and prevented expression of genes that are not normally prevalent in these cells, including HSC-associated and nonlymphoid genes. E2A proteins also restricted proliferation of HSCs, MPPs, and LMPPs and antagonized differentiation of LMPPs toward the myeloid fate. Our results reveal that E2A proteins play a critical role in supporting lymphoid specification from HSCs and that the reduced generation of LMPPs underlies the severe lymphocyte deficiencies observed in E2A-deficient mice. © 2008 Elsevier Inc. All rights reserved.

  • 5.
    Glaros, Vassilis
    et al.
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Rauschmeier, Rene
    Vienna Bioctr VBC, Austria.
    Artemov, Artem V
    Med Univ Vienna, Austria; Endocrinol Res Ctr, Russia.
    Reinhardt, Annika
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Ols, Sebastian
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Emmanouilidi, Aikaterini
    Univ Gothenburg, Sweden.
    Gustafsson, Charlotte
    Karolinska Inst, Sweden.
    You, Yuanyuan
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Mirabello, Claudio
    Linköping University, Department of Physics, Chemistry and Biology, Bioinformatics. Linköping University, Faculty of Science & Engineering.
    Björklund, Åsa K.
    Uppsala Univ, Sweden.
    Perez, Laurent
    Lausanne Univ Hosp, Switzerland; Univ Lausanne, Switzerland.
    King, Neil P.
    Univ Washington, WA 98195 USA; Univ Washington, WA 98195 USA.
    Mansson, Robert
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Angeletti, Davide
    Univ Gothenburg, Sweden.
    Loré, Karin
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Adameyko, Igor
    Med Univ Vienna, Austria; Karolinska Inst, Sweden.
    Busslinger, Meinrad
    Vienna Bioctr VBC, Austria.
    Kreslavsky, Taras
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Limited access to antigen drives generation of early B cell memory while restraining the plasmablast response2021In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 54, no 9, p. 2005-+Article in journal (Refereed)
    Abstract [en]

    Cell fate decisions during early B cell activation determine the outcome of responses to pathogens and vaccines. We examined the early B cell response to T-dependent antigen in mice by single-cell RNA sequencing. Early after immunization, a homogeneous population of activated precursors (APs) gave rise to a transient wave of plasmablasts (PBs), followed a day later by the emergence of germinal center B cells (GCBCs). Most APs rapidly exited the cell cycle, giving rise to non-GC-derived early memory B cells (eMBCs) that retained an AP-like transcriptional profile. Rapid decline of antigen availability controlled these events; provision of excess antigen precluded cell cycle exit and induced a new wave of PBs. Fate mapping revealed a prominent contribution of eMBCs to the MBC pool. Quiescent cells with an MBC phenotype dominated the early response to immunization in primates. A reservoir of APs/eMBCs may enable rapid readjustment of the immune response when failure to contain a threat is manifested by increased antigen availability.

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  • 6.
    Khounlotham, Manirath
    et al.
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Kim, Wooki
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Peatman, Eric
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Nava, Porfirio
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Medina-Contreras, Oscar
    Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
    Addis, Caroline
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Koch, Stefan
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Fournier, Benedicte
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Nusrat, Asma
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Denning, Timothy L.
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA; Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
    Parkos, Charles A.
    Epithelial Pathobiology and Mucosal Inflammation Research Unit, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis2012In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 37, no 3, p. 563-573Article in journal (Refereed)
    Abstract [en]

    Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis. To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis. Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis. Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-beta-producing CD4(+) T cells in F11r(-/-) mice. Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-beta. Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis. These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise.

  • 7.
    Klawonn, Anna
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Stanford Univ, CA 94305 USA.
    Fritz, Michael
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Univ Ulm, Germany.
    Castany Quintana, Silvia
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Pignatelli, Marco
    NIDA, MD 21224 USA; Washington Univ, MO 63110 USA; Washington Univ, MO 63110 USA.
    Canal, Carla
    Autonomous Univ Barcelona, Spain; Autonomous Univ Barcelona, Spain.
    Similä, Fredrik
    Linköping University, Department of Biomedical and Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Tejeda, Hugo A.
    NIDA, MD 21224 USA.
    Levinsson, Julia
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Jaarola, Maarit
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Jakobsson, Johan
    Lund Univ, Sweden; Lund Univ, Sweden.
    Hidalgo, Juan
    Autonomous Univ Barcelona, Spain; Autonomous Univ Barcelona, Spain.
    Heilig, Markus
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Psykiatricentrum, Psykiatriska kliniken i Linköping.
    Bonci, Antonello
    Global Inst Addict, FL 33132 USA.
    Engblom, David
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Microglial activation elicits a negative affective state through prostaglandin-mediated modulation of striatal neurons2021In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 54, no 2, p. 225-234.e6Article in journal (Refereed)
    Abstract [en]

    Microglia are activated in many neurological diseases and have been suggested to play an important role in the development of affective disorders including major depression. To investigate how microglial signaling regulates mood, we used bidirectional chemogenetic manipulations of microglial activity in mice. Activation of microglia in the dorsal striatum induced local cytokine expression and a negative affective state characterized by anhedonia and aversion, whereas inactivation of microglia blocked aversion induced by systemic inflammation. Interleukin-6 signaling and cyclooxygenase-1 mediated prostaglandin synthesis in the microglia were critical for the inflammation-induced aversion. Correspondingly, microglial activation led to a prostaglandin-dependent reduction of the excitability of striatal neurons. These findings demonstrate a mechanism by which microglial activation causes negative affect through prostaglandin-dependent modulation of striatal neurons and indicate that interference with this mechanism could milden the depressive symptoms in somatic and psychiatric diseases involving microglial activation.

  • 8.
    Lanca, Telma
    et al.
    Tech Univ Denmark, Denmark.
    Ungerback, Jonas
    Lund Univ, Sweden.
    Da Silva, Clement
    Lund Univ, Sweden.
    Joeris, Thorsten
    Lund Univ, Sweden.
    Ahmadi, Fatemeh
    Lund Univ, Sweden.
    Vandamme, Julien
    Tech Univ Denmark, Denmark.
    Svensson-Frej, Marcus
    Tech Univ Denmark, Denmark.
    Mowat, Allan Mci
    Univ Glasgow, Scotland.
    Kotarsky, Knut
    Lund Univ, Sweden.
    Sigvardsson, Mikael
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences. Lund Univ, Sweden.
    Agace, William W.
    Tech Univ Denmark, Denmark; Lund Univ, Sweden.
    IRF8 deficiency induces the transcriptional, functional, and epigenetic reprogramming of cDC1 into the cDC2 lineage2022In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 55, no 8, p. 1431-1447.e11Article in journal (Refereed)
    Abstract [en]

    Conventional dendritic cells (cDCs) consist of two major functionally and phenotypically distinct subsets, cDC1 and cDC2, whose development is dependent on distinct sets of transcription factors. Interferon regulatory factor 8 (IRF8) is required at multiple stages of cDC1 development, but its role in committed cDC1 remains unclear. Here, we used Xcr1-cre to delete Irf8 in committed cDC1 and demonstrate that Irf8 is required for maintaining the identity of cDC1. In the absence of Irf8, committed cDC1 acquired the transcriptional, functional, and chromatin accessibility properties of cDC2. This conversion was independent of Irf4 and was associated with the decreased accessibility of putative IRF8, Batf3, and composite AP-1-IRF (AICE)-binding elements, together with increased accessibility of cDC2-associated transcription-factor-binding elements. Thus, IRF8 expression by committed cDC1 is required for preventing their conversion into cDC2-like cells.

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  • 9.
    Los, Marek Jan
    et al.
    Department of Internal Medicine I, Medical Clinics, University of Tübingen, D72076 Tübingen, Germany.
    Wesselborg, S.
    Department of Internal Medicine I, Medical Clinics, University of Tübingen, D72076 Tübingen, Germany.
    Schulze-Osthoff, K.
    Department of Internal Medicine I, Medical Clinics, University of Tübingen, D72076 Tübingen, Germany.
    The role of caspases in development, immunity, and apoptotic signal transduction: Lessons from knockout mice1999In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 10, no 6, p. 629-639Article, review/survey (Refereed)
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  • 10.
    Mercer, Elinore M
    et al.
    University of California San Diego.
    Lin, Yin C
    University of California San Diego.
    Benner, Christopher
    University of California San Diego.
    Jhunjhunwala, Suchit
    University of California San Diego.
    Dutkowski, Janusz
    University of California San Diego.
    Flores, Martha
    University of California San Diego.
    Sigvardsson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Experimental Hematology. Linköping University, Faculty of Health Sciences.
    Ideker, Trey
    University of California San Diego.
    Glass, Christopher K
    University of California San Diego.
    Murre, Cornelis
    University of California San Diego.
    Multilineage Priming of Enhancer Repertoires Precedes Commitment to the B and Myeloid Cell Lineages in Hematopoietic Progenitors2011In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 35, no 3, p. 413-425Article in journal (Refereed)
    Abstract [en]

    Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A (Tcf3) in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are premarked by the poised or active enhancer mark H3K4me1 in multipotent progenitors. Thus, in hematopoietic progenitors, multilineage priming of enhancer elements precedes commitment to the lymphoid or myeloid cell lineages.

  • 11.
    Mjösberg, Jenny
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Karolinska Institute, Sweden.
    Mazzurana, Luca
    Karolinska Institute, Sweden.
    Editorial Material: ILC-poiesis: Making Tissue ILCs from Blood in IMMUNITY, vol 46, issue 3, pp 344-3462017In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 46, no 3, p. 344-346Article in journal (Other academic)
    Abstract [en]

    n/a

  • 12.
    Månsson, Robert
    et al.
    Lund University.
    Hultquist, Anne
    Lund University.
    Luc, Sidinh
    Lund University.
    Yang, Liping
    Lund University.
    Anderson, Kristina
    Lund University.
    Kharazi, Shabnam
    Lund University.
    Al-Hashmi, Suleiman
    Lund University.
    Liuba, Karina
    Lund University.
    Thorén, Lina
    Lund University.
    Adolfsson, Jörgen
    Lund University.
    Buza-Vidas, Natalija
    Lund University.
    Qian, Hong
    Lund University.
    Soneji, Shamit
    University of Oxford.
    Enver, Tariq
    University of Oxford.
    Sigvardsson, Mikael
    Lund University.
    Jacobsen, Sten Eirik W
    Lund University.
    Molecular evidence for hierarchical transcriptional lineage priming in fetal and adult stem cells and multipotent progenitors2007In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 26, no 4, p. 407-419Article in journal (Refereed)
    Abstract [en]

    Recent studies implicated the existence of adult lymphoid-primed multipotent progenitors (LMPPs) with little or no megakaryocyte-erythroid potential, questioning common myeloid and lymphoid progenitors as obligate intermediates in hematopoietic stem cell (HSC) lineage commitment. However, the existence of LMPPs remains contentious. Herein, global and single-cell analyses revealed a hierarchical organization of transcriptional lineage programs, with downregulation of megakaryocyte-erythroid genes from HSCs to LMPPs, sustained granulocyte-monocyte priming, and upregulation of common lymphoid (but not B and T cell-specific) genes. These biological and molecular relationships, implicating almost mutual exclusion of megakaryocyte-erythroid and lymphoid pathways, are established already in fetal hematopoiesis, as evidenced by existence of LMPPs in fetal liver. The identification of LMPPs and hierarchically ordered transcriptional activation and downregulation of distinct lineage programs is compatible with a model for HSC lineage commitment in which the probability for undergoing different lineage commitment fates changes gradually when progressing from HSCs to LMPPs.

  • 13.
    Nava, Porfirio
    et al.
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Koch, Stefan
    Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Laukoetter, Mike G.
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA; Department of General Surgery, Universitaet Muenster, Muenster, Germany.
    Lee, Winston Y.
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Kolegraff, Keli
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Capaldo, Christopher T.
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Beeman, Neal
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Addis, Caroline
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Gerner-Smidt, Kirsten
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Neumaier, Irmgard
    Biologische Chemie, Technische Universitaet Muenchen, Freising-Weihenstephan, Germany.
    Skerra, Arne
    Biologische Chemie, Technische Universitaet Muenchen, Freising-Weihenstephan, Germany.
    Li, Linheng
    Stowers Institute for Medical Research, Kansas City, MO, USA.
    Parkos, Charles A.
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Nusrat, Asma
    Epithelial Pathobiology Unit, Department of Pathology & Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA.
    Interferon-gamma regulates intestinal epithelial homeostasis through converging beta-catenin signaling pathways2010In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 32, no 3, p. 392-402Article in journal (Refereed)
    Abstract [en]

    Inflammatory cytokines have been proposed to regulate epithelial homeostasis during intestinal inflammation. We report here that interferon-gamma (IFN-gamma) regulates the crucial homeostatic functions of cell proliferation and apoptosis through serine-threonine protein kinase AKT-beta-catenin and Wingless-Int (Wnt)-beta-catenin signaling pathways. Short-term exposure of intestinal epithelial cells to IFN-gamma resulted in activation of beta-catenin through AKT, followed by induction of the secreted Wnt inhibitor Dkk1. Consequently, we observed an increase in Dkk1-mediated apoptosis upon extended IFN-gamma treatment and reduced proliferation through depletion of the Wnt coreceptor LRP6. These effects were enhanced by tumor necrosis factor-alpha (TNF-alpha), suggesting synergism between the two cytokines. Consistent with these results, colitis in vivo was associated with decreased beta-catenin-T cell factor (TCF) signaling, loss of plasma membrane-associated LRP6, and reduced epithelial cell proliferation. Proliferation was partially restored in IFN-gamma-deficient mice. Thus, we propose that IFN-gamma regulates intestinal epithelial homeostasis by sequential regulation of converging beta-catenin signaling pathways.

  • 14.
    Ramirez, Kevin
    et al.
    University of Chicago, USA .
    Chandler, Katherine J.
    University of Utah, USA .
    Spaulding, Christina
    University of Chicago, 15 USA .
    Zandi, Sasan
    Linköping University, Department of Clinical and Experimental Medicine, Experimental Hematology. Linköping University, Faculty of Health Sciences.
    Sigvardsson, Mikael
    Linköping University, Department of Clinical and Experimental Medicine, Experimental Hematology. Linköping University, Faculty of Health Sciences.
    Graves, Barbara J.
    University of Utah, USA .
    Kee, Barbara L.
    University of Chicago, USA .
    Gene Deregulation and Chronic Activation in Natural Killer Cells Deficient in the Transcription Factor ETS12012In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 36, no 6, p. 921-932Article in journal (Refereed)
    Abstract [en]

    Multiple transcription factors guide the development of mature functional natural killer (NK) cells, yet little is known about their function. We used global gene expression and genome-wide binding analyses combined with developmental and functional studies to unveil three roles for the ETS1 transcription factor in NK cells. ETS1 functions at the earliest stages of NK cell development to promote expression of critical transcriptional regulators including T-BET and ID2, NK cell receptors (NKRs) including NKp46, Ly49H, and Ly49D, and signaling molecules essential for NKR function. As a consequence, Ets(-/-) NK cells fail to degranulate after stimulation through activating NKRs. Nonetheless, these cells are hyperresponsive to cytokines and have characteristics of chronic stimulation including increased expression of inhibitory NKRs and multiple activation-associated genes. Therefore, ETS1 regulates a broad gene expression program in NK cells that promotes target cell recognition while limiting cytokine-driven activation.

  • 15.
    Zitti, Beatrice
    et al.
    Karolinska Inst, Sweden.
    Hoffer, Elena
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden; Univ Copenhagen, Denmark.
    Zheng, Wenning
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden; Univ Copenhagen, Denmark.
    Pandey, Ram Vinay
    Karolinska Inst, Sweden.
    Schlums, Heinrich
    Karolinska Inst, Sweden.
    Casoni, Giovanna Perinetti
    Karolinska Inst, Sweden.
    Fusi, Irene
    Karolinska Inst, Sweden; Univ Siena, Italy.
    Nguyen, Lien
    Karolinska Inst, Sweden.
    Karner, Jaanika
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Kokkinou, Efthymia
    Karolinska Inst, Sweden.
    Carrasco, Anna
    Karolinska Inst, Sweden.
    Gahm, Jessica
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Ehrstrom, Marcus
    Nordiska Kliniken, Sweden.
    Happaniemi, Staffan
    Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Norrköping.
    Keita, Åsa
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Hedin, Charlotte R. H.
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Mjosberg, Jenny
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Eidsmo, Liv
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden; Univ Copenhagen, Denmark.
    Bryceson, Yenan T.
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden; Univ Bergen, Norway.
    Human skin-resident CD8+T cells require RUNX2 and RUNX3 for induction of cytotoxicity and expression of the integrin CD49a2023In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 56, no 6, p. 1285-1302.e7Article in journal (Refereed)
    Abstract [en]

    The integrin CD49a marks highly cytotoxic epidermal-tissue-resident memory (TRM) cells, but their differen-tiation from circulating populations remains poorly defined. We demonstrate enrichment of RUNT family tran-scription-factor-binding motifs in human epidermal CD8+CD103+CD49a+ TRM cells, paralleled by high RUNX2 and RUNX3 protein expression. Sequencing of paired skin and blood samples revealed clonal overlap be-tween epidermal CD8+CD103+CD49a+ TRM cells and circulating memory CD8+CD45RA-CD62L+ T cells. In vitro stimulation of circulating CD8+CD45RA-CD62L+ T cells with IL-15 and TGF-b induced CD49a expres-sion and cytotoxic transcriptional profiles in a RUNX2-and RUNX3-dependent manner. We therefore identi-fied a reservoir of circulating cells with cytotoxic TRM potential. In melanoma patients, high RUNX2, but not RUNX3, transcription correlated with a cytotoxic CD8+CD103+CD49a+ TRM cell signature and improved pa-tient survival. Together, our results indicate that combined RUNX2 and RUNX3 activity promotes the differ-entiation of cytotoxic CD8+CD103+CD49a+ TRM cells, providing immunosurveillance of infected and malig-nant cells.

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