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  • 1
    Language: English
    In: Immunity, 14 November 2013, Vol.39(5), pp.797-799
    Description: The transcription factor IRF4 is known to be essential for differentiation of effector CD4 T cell subsets. In this issue, identify IRF4 as a regulator of checkpoints in the final steps and maintenance of CD8 T cell effector differentiation.
    Keywords: Medicine ; Biology
    ISSN: 1074-7613
    E-ISSN: 1097-4180
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  • 2
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 10 September 2013, Vol.110(37), pp.15019-24
    Description: Robust cytotoxic CD8(+) T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8(+) T-cell response to the intracellular bacterium Listeria monocytogenes. IRF4-deficient (Irf4(-/-)) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes-specific CD8(+) T cells with impaired effector phenotype and function. Transfer of wild-type CD8(+) T cells into Irf4(-/-) mice improved bacterial clearance, suggesting an intrinsic defect of CD8(+) T cells in Irf4(-/-) mice. Following transfer into wild-type recipients, Irf4(-/-) CD8(+) T cells became activated and showed initial proliferation upon L. monocytogenes infection. However, these cells could not sustain proliferation, produced reduced amounts of IFN-γ and TNF-α, and failed to acquire cytotoxic function. Forced IRF4 expression in Irf4(-/-) CD8(+) T cells rescued the defect. During acute infection, Irf4(-/-) CD8(+) T cells demonstrated diminished expression of B lymphocyte-induced maturation protein-1 (Blimp-1), inhibitor of DNA binding (Id)2, and T-box expressed in T cells (T-bet), transcription factors programming effector-cell generation. IRF4 was essential for expression of Blimp-1, suggesting that altered regulation of Blimp-1 contributes to the defects of Irf4(-/-) CD8(+) T cells. Despite increased levels of B-cell lymphoma 6 (BCL-6), Eomesodermin, and Id3, Irf4(-/-) CD8(+) T cells showed impaired memory-cell formation, indicating additional functions for IRF4 in this process. As IRF4 governs B-cell and CD4(+) T-cell differentiation, the identification of its decisive role in peripheral CD8(+) T-cell differentiation, suggests a common regulatory function for IRF4 in adaptive lymphocytes fate decision.
    Keywords: Interferon Regulatory Factors -- Immunology ; T-Lymphocytes, Cytotoxic -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 30 December 2008, Vol.105(52), pp.20846-51
    Description: Differentiation of murine T-helper (Th) 17 cells is induced by antigenic stimulation and the sequential action of the cytokines IL-6, IL-21, and IL-23, along with TGFbeta. Current dogma proposes that IL-6 induces IL-21, which, in a STAT3-dependent manner, amplifies its own transcription, contributes to IL-17 production, and, moreover, promotes the expression of the IL-23 receptor. This, in turn, prepares cells for IL-23-mediated stabilization of the Th17 phenotype. Here we demonstrate that these effects of IL-21 on Th17 differentiation are completely dependent on IFN regulatory factor 4 (IRF4). After culturing in the presence of IL-21 plus TGFbeta, IRF4-deficient (Irf4(-/-)) Th cells showed a profound intrinsic defect in IL-17 production and in the autocrine IL-21 loop. Likewise, the levels of IL-23 receptor and the lineage-specific orphan nuclear receptors RORalpha and RORgammat were diminished, whereas the T regulatory (Treg) transcription factor forkhead box P3 (Foxp3) was strongly up-regulated, consistent with the reciprocal relationship between Th17 and Treg development. Despite this loss of IL-21 functions, IL-21-induced STAT3 activation was unimpaired and induced normal Socs3 expression. Forced expression of Foxp3 in WT cells inhibited IL-21-mediated IL-17 production, suggesting that the increase in Foxp3 contributes to the Irf4(-/-) phenotype. Additionally, the low levels of RORalpha and RORgammat are also partially responsible, because simultaneous overexpression of both proteins restored IL-17 production in Irf4(-/-) cells to some extent. These data highlight IRF4 as a decisive factor during the IL-21-mediated steps of Th17 development by influencing the balance of Foxp3, RORalpha, and RORgammat.
    Keywords: Autocrine Communication -- Immunology ; Interferon Regulatory Factors -- Immunology ; Interleukins -- Immunology ; T-Lymphocytes, Helper-Inducer -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 29 May 2012, Vol.109(22), pp.8664-9
    Description: Follicular T-helper (T(FH)) cells cooperate with GL7(+)CD95(+) germinal center (GC) B cells to induce antibody maturation. Herein, we identify the transcription factor IRF4 as a T-cell intrinsic precondition for T(FH) cell differentiation and GC formation. After immunization with protein or infection with the protozoon Leishmania major, draining lymph nodes (LNs) of IFN-regulatory factor-4 (Irf4(-/-)) mice lacked GCs and GC B cells despite developing normal initial hyperplasia. GCs were also absent in Peyer's patches of naive Irf4(-/-) mice. Accordingly, CD4(+) T cells within the LNs and Peyer's patches failed to express the T(FH) key transcription factor B-cell lymphoma-6 and other T(FH)-related molecules. During chronic leishmaniasis, the draining Irf4(-/-) LNs disappeared because of massive cell death. Adoptive transfer of WT CD4(+) T cells or few L. major primed WT T(FH) cells reconstituted GC formation, GC B-cell differentiation, and LN cell survival. In support of a T-cell intrinsic IRF4 activity, Irf4(-/-) T(FH) cell differentiation was not rescued by close neighborhood to transferred WT T(FH) cells. Together with its known B lineage-specific roles during plasma cell maturation and class switch, our study places IRF4 in the center of antibody production toward T-cell-dependent antigens.
    Keywords: Cell Differentiation -- Immunology ; Germinal Center -- Immunology ; Interferon Regulatory Factors -- Immunology ; T-Lymphocytes, Helper-Inducer -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: Cancer Research, 07/15/2016, Vol.76(14 Supplement), pp.1594-1594
    Description: The tumor microenvironment and its immune components play a critical role in cancer development, progression, and control. In this study we aim to investigate the role of tumor infiltrating lymphocyte subpopulations in lung cancer progression.
    Keywords: Metastases ; Microenvironments ; Lymphocytes ; Tumors ; Mesenchyme ; Lung Cancer ; Cancer Immunology;
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
    Language: German
    In: Allergo Journal, 2015, Vol.24(1), pp.24-31
    Description: Die Aktivierung naiver CD4+ und CD8+ T-Zellen als Antwort auf Antigene und ihre anschließende Proliferation und Differenzierung zu Effektorzellen sind wichtige Funktionen der zellvermittelten Immunantwort. CD4+ T-Zellen (auch bekannt als T-Helferzellen, Th) differenzieren in verschiedene Subpopulationen, einschließlich Th1, Th2, Th9, Th17, Tfh und regulatorische T-Zellen (Treg). Diese werden durch spezifische Zytokinprofile und Effektorfunktionen charakterisiert. Neuere Daten zeigen, dass sich auch CD8+ T-Zellen (zytotoxische T-Lymphozyten (CTL), oder Tc-Zellen) zu Subpopulationen mit ähnlichen Merkmalen entwickeln können. So sind neben CTLs auch Tc2, Tc9, Tc17 und CD8+ Treg-Zellen bekannt. Obwohl diese Subpopulationen wichtige Schutzfunktionen erfüllen, kann eine unkontrollierte Immunantwort pathologisch sein und Allergie oder Autoimmunität verursachen. Unsere jüngsten Ergebnisse implizieren eine Änderung des gegenwärtigen Paradigmas im Rahmen dieser immunpathologischen Prozesse. Es zeigt sich, dass manche CD8+ T-Zell-Subpopulationen, statt zytotoxisch zu sein, eher als wirksame Helfer der Aktivierung von CD4+ T-Zellen agieren. In dieser Übersichtsarbeit fokussieren wir uns auf die Rolle der Th2-, Th9-, Th17- sowie der Tc9- und Tc17-Zellen während allergischem Asthma und autoimmuner Encephalomyelitis sowie auf ihre Kooperation im Rahmen dieser pathologischen Immunreaktionen. Huber M, Lohoff M. Change of paradigm: CD8+ T cells as important helper for CD4+ T cells during asthma and autoimmune encephalomyelitis. Allergo J Int 2015;24:8–15
    Keywords: Medicine & Public Health ; General Practice / Family Medicine ; Allergology ; Cd4+ T-Zellen ; Cd8+ T-Zellen ; Asthma ; Autoimmune Encephalomyelitis;
    ISSN: 0941-8849
    E-ISSN: 2195-6405
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  • 7
    Language: English
    In: International Journal of Medical Microbiology, Oct, 2012, Vol.302(4-5), p.230(6)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ijmm.2012.07.006 Byline: Katharina Reinhard, Magdalena Huber, Michael Lohoff, Alexander Visekruna Keywords: NF-[kappa]B; Signal transduction; Leishmania infection; Cytokines; Toll-like receptors Abstract: Members of the nuclear factor-[kappa]B (NF-[kappa]B) family of transcription factors regulate a variety of molecules involved in host defense against pathogens. A prominent role of NF-[kappa]B in innate and adoptive immunity is based on the regulation of inducible transcription of various genes whose products are essential components of the immune response such as cytokines, chemokines, and adhesion molecules. Since the discovery of the five members of the NF-[kappa]B transcription factor family, RelA, c-Rel, RelB, p50 and p52, considerable progress has been made toward better understanding how the different NF-[kappa]B homo- and heterodimers regulate such distinct subsets of target genes. All of the NF-[kappa]B molecules are activated by various infectious stimuli; however, there are still open questions related to the selective functions of individual NF-[kappa]B family members during a coordinated immune response to infection. Diverse parasites such as Toxoplasma gondii, Leishmania donovani, Leishmania major, and Trichuris muris have been reported to activate NF-[kappa]B signaling cascades, and a number of distinct parasite-derived molecules may actively interfere with the pathways that lead to NF-[kappa]B activation. In this review, we provide an overview on the role of NF-[kappa]B activation in leishmaniasis and discuss how individual NF-[kappa]B family members might perform their distinct and non-overlapping functions in the regulation of protective immunity to Leishmania infection. Author Affiliation: Institute for Medical Microbiology and Hygiene, University of Marburg, Hans Meerwein Stra[sz]e 2, 35032 Marburg, Germany
    Keywords: Transcription (Genetics) -- Health Aspects
    ISSN: 1438-4221
    Source: Cengage Learning, Inc.
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  • 8
    Language: English
    In: Allergo Journal International, 2015, Vol.24(1), pp.8-15
    Description: The activation of naive CD4+ and CD8+ T cells in response to antigen and their subsequent proliferation and differentiation into effectors are important features of a cell-mediated immune response. CD4+ T cells (also known as T helper cells, Th) differentiate into several subpopulations including Th1, Th2, Th9, Th17, Tfh and Treg cells, characterized by specific cytokine profiles and effector functions. However, recent evidence indicates that CD8+ T cells (termed cytotoxic T lymphocytes, CTLs or Tc cells) can differentiate into subpopulations with similar characteristics denoted as Tc2, Tc9, Tc17 and CD8+ Treg cells in addition to CTLs. Although these subpopulations accomplish important protective functions, their uncontrolled responses cause immunopathology including allergy and autoimmunity. Our recent findings indicate a change of paradigm: during these pathologic responses, CD8+ T cell subpopulations act as strong helpers for the activity of CD4+ T cells rather than being cytotoxic. In this review, we focus on the role of Th2, Th9, Th17 as well as Tc9 and Tc17 cells in asthma and autoimmune encephalomyelitis and on their interaction during these immunopathologic responses. Huber M, Lohoff M. Change of paradigm: CD8+ T cells as important helper for CD4+ T cells during asthma and autoimmune encephalomyelitis. Allergo J Int 2015;24:8–15
    Keywords: CD4+ T cells ; CD8+ T cells ; asthma ; autoimmune encephalomyelitis
    E-ISSN: 2197-0378
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  • 9
    Language: English
    In: Cytokine, 2014, Vol.70(1), p.47
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cyto.2014.07.087 Byline: Magdalena Huber, Magdalena Suprunenko, Eric Tran, Markus Eickmann, Claudia Weiss, Campbell L. Iain, Markus J. Hofer Abstract: Functional type I interferon (IFN-I) signalling is critical for the host response to viruses. Cellular responses IFN-Is depend largely on STAT1, STAT2 and IRF9. Here we studied the effects of IRF9-deficiency on the host response to a viral infection in the CNS. Wild-type (WT) mice and mice lacking IRF9 (IRF9 KO) were infected intracranially with lymphocytic choriomeningitis virus (LCMV). In WT mice, lethal disease occurred by day 7 with characteristic cerebral seizures and LCMV being largely confined to the CNS. In contrast, LCMV-infection of IRF9 KO mice caused a transient non-fatal disease and virus spread to peripheral organs. Viral RNA levels decreased slowly over time and became undetectable in some peripheral organs such as liver and spleen but remained detectable in the CNS for more than 150days. In the CNS, sites of viral infection were associated with foci of activated microglia/ macrophages and moderate T-cell infiltrates. The persistent infection in the CNS and peripheral organs was paralleled by significantly increased levels of various cytokine mRNAs, including IFN-g and TNF, as well as of the co-inhibitory molecule B7-H1 (or PD-L1). In conclusion, these findings indicate that the absence of IRF9 prevents lethal LCM but results in persistent infection and chronic inflammation in the CNS. The presence of T cells and the slow decrease in viral RNA levels in the CNS and peripheral organs argue for a retarded rather than an exhausted or incapacitated anti-viral response.
    Keywords: Biological Response Modifiers – Health Aspects ; Virus Diseases – Health Aspects ; Antiviral Agents – Health Aspects
    ISSN: 1043-4666
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: Cancer research, 01 November 2018, Vol.78(21), pp.6223-6234
    Description: Plasmacytoid dendritic cells (pDC) are the main producers of a key T-cell-stimulatory cytokine, IFNα, and critical regulators of antiviral immunity. Chronic myeloid leukemia (CML) is caused by BCR-ABL, which is an oncogenic tyrosine kinase that can be effectively inhibited with ABL-selective tyrosine kinase inhibitors (TKI). BCR-ABL-induced suppression of the transcription factor interferon regulatory factor 8 was previously proposed to block pDC development and compromise immune surveillance in CML. Here, we demonstrate that pDCs in newly diagnosed CML (CML-pDC) develop quantitatively normal and are frequently positive for the costimulatory antigen CD86. They originate from low-level -expressing precursors. CML-pDCs also retain their competence to maturate and to secrete IFN. RNA sequencing reveals a strong inflammatory gene expression signature in CML-pDCs. Patients with high CML-pDC counts at diagnosis achieve inferior rates of deep molecular remission (MR) under nilotinib, unless nilotinib therapy is combined with IFN, which strongly suppresses circulating pDC counts. Although most pDCs are -negative in MR, a substantial proportion of CML-pDCs persists under TKI treatment. This could be of relevance, because CML-pDCs elicit CD8 T cells, which protect wild-type mice from CML. Together, pDCs are identified as novel functional DC population in CML, regulating antileukemic immunity and treatment outcome in CML. CML-pDC originates from low-level BCR-ABL expressing stem cells into a functional immunogenic DC-population regulating antileukemic immunity and treatment outcome in CML. .
    Keywords: Dendritic Cells -- Cytology ; Leukemia, Myelogenous, Chronic, BCR-Abl Positive -- Pathology
    ISSN: 00085472
    E-ISSN: 1538-7445
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