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  • 1
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    Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: Chronic infections strain the regenerative capacity of antiviral T lymphocyte populations, leading to failure in long-term immunity. The cellular and molecular events controlling this regenerative capacity, however, are unknown. We found that two distinct states of virus-specific CD8(+) T cells exist in chronically infected mice and humans. Differential expression of the T-box transcription factors T-bet and Eomesodermin (Eomes) facilitated the cooperative maintenance of the pool of antiviral CD8(+) T cells during chronic viral infection. T-bet(hi) cells displayed low intrinsic turnover but proliferated in response to persisting antigen, giving rise to Eomes(hi) terminal progeny. Genetic elimination of either subset resulted in failure to control chronic infection, which suggests that an imbalance in differentiation and renewal could underlie the collapse of immunity in humans with chronic infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653769/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3653769/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paley, Michael A -- Kroy, Daniela C -- Odorizzi, Pamela M -- Johnnidis, Jonathan B -- Dolfi, Douglas V -- Barnett, Burton E -- Bikoff, Elizabeth K -- Robertson, Elizabeth J -- Lauer, Georg M -- Reiner, Steven L -- Wherry, E John -- 059312/Wellcome Trust/United Kingdom -- AI061699/AI/NIAID NIH HHS/ -- AI0663445/AI/NIAID NIH HHS/ -- AI076458/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- HHSN266200500030C/AI/NIAID NIH HHS/ -- HHSN266200500030C/PHS HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P30 CA016520/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI042370/AI/NIAID NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- R01 AI076458/AI/NIAID NIH HHS/ -- T32 AI007632/AI/NIAID NIH HHS/ -- T32-AI-07324/AI/NIAID NIH HHS/ -- U19 AI082630/AI/NIAID NIH HHS/ -- U19 AI083022/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1220-5. doi: 10.1126/science.1229620.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Hepatitis B, Chronic/*immunology ; Humans ; Liver/virology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Stem Cells/immunology ; T-Box Domain Proteins/genetics/*metabolism ; T-Lymphocyte Subsets/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Immunology. An interferon paradox (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-04-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Odorizzi, Pamela M -- Wherry, E John -- T32 AI007632/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):155-6. doi: 10.1126/science.1237568.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology and Department of Microbiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arenaviridae Infections/*immunology/*virology ; Female ; Interferon Type I/*immunology/*metabolism ; Lymphocytic choriomeningitis virus/*immunology/*physiology ; Male ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    TSLP promotes interleukin-3-independent basophil haematopoiesis and type 2 inflammation (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-16
    Description: CD4(+) T-helper type 2 (T(H)2) cells, characterized by their expression of interleukin (IL)-4, IL-5, IL-9 and IL-13, are required for immunity to helminth parasites and promote the pathological inflammation associated with asthma and allergic diseases. Polymorphisms in the gene encoding the cytokine thymic stromal lymphopoietin (TSLP) are associated with the development of multiple allergic disorders in humans, indicating that TSLP is a critical regulator of T(H)2 cytokine-associated inflammatory diseases. In support of genetic analyses, exaggerated TSLP production is associated with asthma, atopic dermatitis and food allergies in patients, and studies in murine systems demonstrated that TSLP promotes T(H)2 cytokine-mediated immunity and inflammation. However, the mechanisms through which TSLP induces T(H)2 cytokine responses remain poorly defined. Here we demonstrate that TSLP promotes systemic basophilia, that disruption of TSLP-TSLPR interactions results in defective basophil responses, and that TSLPR-sufficient basophils can restore T(H)2-cell-dependent immunity in vivo. TSLP acted directly on bone-marrow-resident progenitors to promote basophil responses selectively. Critically, TSLP could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and genome-wide transcriptional profiling and functional analyses identified heterogeneity between TSLP-elicited versus IL-3-elicited basophils. Furthermore, activated human basophils expressed TSLPR, and basophils isolated from eosinophilic oesophagitis patients were distinct from classical basophils. Collectively, these studies identify previously unrecognized heterogeneity within the basophil cell lineage and indicate that expression of TSLP may influence susceptibility to multiple allergic diseases by regulating basophil haematopoiesis and eliciting a population of functionally distinct basophils that promote T(H)2 cytokine-mediated inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263308/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263308/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siracusa, Mark C -- Saenz, Steven A -- Hill, David A -- Kim, Brian S -- Headley, Mark B -- Doering, Travis A -- Wherry, E John -- Jessup, Heidi K -- Siegel, Lori A -- Kambayashi, Taku -- Dudek, Emily C -- Kubo, Masato -- Cianferoni, Antonella -- Spergel, Jonathan M -- Ziegler, Steven F -- Comeau, Michael R -- Artis, David -- AI083480/AI/NIAID NIH HHS/ -- AI61570/AI/NIAID NIH HHS/ -- AI74878/AI/NIAID NIH HHS/ -- AI87990/AI/NIAID NIH HHS/ -- F31 GM082187/GM/NIGMS NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI061570-09/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI074878-05/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI095466-02/AI/NIAID NIH HHS/ -- R01 HL107589/HL/NHLBI NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI083480-02/AI/NIAID NIH HHS/ -- T32 AI060516/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- U01 AI095608-02/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 14;477(7363):229-33. doi: 10.1038/nature10329.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21841801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology ; Basophils/*cytology/metabolism ; Cytokines/genetics/immunology/*metabolism ; Dermatitis, Atopic/immunology ; Food Hypersensitivity/immunology ; *Hematopoiesis ; Humans ; Hypersensitivity, Immediate/*immunology ; Inflammation/*immunology/*metabolism ; *Interleukin-3/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Phenotype ; Receptors, Cytokine/metabolism ; Receptors, Interleukin-3/deficiency/genetics/metabolism ; Th2 Cells/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-05-24
    Description: Innate lymphoid cells (ILCs) are a recently characterized family of immune cells that have critical roles in cytokine-mediated regulation of intestinal epithelial cell barrier integrity. Alterations in ILC responses are associated with multiple chronic human diseases, including inflammatory bowel disease, implicating a role for ILCs in disease pathogenesis. Owing to an inability to target ILCs selectively, experimental studies assessing ILC function have predominantly used mice lacking adaptive immune cells. However, in lymphocyte-sufficient hosts ILCs are vastly outnumbered by CD4(+) T cells, which express similar profiles of effector cytokines. Therefore, the function of ILCs in the presence of adaptive immunity and their potential to influence adaptive immune cell responses remain unknown. To test this, we used genetic or antibody-mediated depletion strategies to target murine ILCs in the presence of an adaptive immune system. We show that loss of retinoic-acid-receptor-related orphan receptor-gammat-positive (RORgammat(+)) ILCs was associated with dysregulated adaptive immune cell responses against commensal bacteria and low-grade systemic inflammation. Remarkably, ILC-mediated regulation of adaptive immune cells occurred independently of interleukin (IL)-17A, IL-22 or IL-23. Genome-wide transcriptional profiling and functional analyses revealed that RORgammat(+) ILCs express major histocompatibility complex class II (MHCII) and can process and present antigen. However, rather than inducing T-cell proliferation, ILCs acted to limit commensal bacteria-specific CD4(+) T-cell responses. Consistent with this, selective deletion of MHCII in murine RORgammat(+) ILCs resulted in dysregulated commensal bacteria-dependent CD4(+) T-cell responses that promoted spontaneous intestinal inflammation. These data identify that ILCs maintain intestinal homeostasis through MHCII-dependent interactions with CD4(+) T cells that limit pathological adaptive immune cell responses to commensal bacteria.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699860/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hepworth, Matthew R -- Monticelli, Laurel A -- Fung, Thomas C -- Ziegler, Carly G K -- Grunberg, Stephanie -- Sinha, Rohini -- Mantegazza, Adriana R -- Ma, Hak-Ling -- Crawford, Alison -- Angelosanto, Jill M -- Wherry, E John -- Koni, Pandelakis A -- Bushman, Frederic D -- Elson, Charles O -- Eberl, Gerard -- Artis, David -- Sonnenberg, Gregory F -- 2-P30 CA016520/CA/NCI NIH HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI095776/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- DK071176/DK/NIDDK NIH HHS/ -- DP5 OD012116/OD/NIH HHS/ -- DP5OD012116/OD/NIH HHS/ -- P01 DK071176/DK/NIDDK NIH HHS/ -- P30 DK050306/DK/NIDDK NIH HHS/ -- P30DK50306/DK/NIDDK NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32 AI007532/AI/NIAID NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- T32-AI055428/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Jun 6;498(7452):113-7. doi: 10.1038/nature12240. Epub 2013 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23698371" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation/immunology ; Bacteria/*immunology ; CD4-Positive T-Lymphocytes/cytology/*immunology/pathology ; Cell Proliferation ; Histocompatibility Antigens Class II/immunology/metabolism ; Humans ; Immunity, Innate/*immunology ; Inflammation/pathology ; Interleukin-17/metabolism ; Interleukin-23/metabolism ; Interleukins/metabolism ; Intestines/*immunology/*microbiology/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; *Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-02
    Description: The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548887/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osborne, Lisa C -- Monticelli, Laurel A -- Nice, Timothy J -- Sutherland, Tara E -- Siracusa, Mark C -- Hepworth, Matthew R -- Tomov, Vesselin T -- Kobuley, Dmytro -- Tran, Sara V -- Bittinger, Kyle -- Bailey, Aubrey G -- Laughlin, Alice L -- Boucher, Jean-Luc -- Wherry, E John -- Bushman, Frederic D -- Allen, Judith E -- Virgin, Herbert W -- Artis, David -- 095831/Wellcome Trust/United Kingdom -- 2-P30 CA016520/CA/NCI NIH HHS/ -- 5T32A100716334/PHS HHS/ -- AI061570/AI/NIAID NIH HHS/ -- AI074878/AI/NIAID NIH HHS/ -- AI082630/AI/NIAID NIH HHS/ -- AI083022/AI/NIAID NIH HHS/ -- AI087990/AI/NIAID NIH HHS/ -- AI095466/AI/NIAID NIH HHS/ -- AI095608/AI/NIAID NIH HHS/ -- AI097333/AI/NIAID NIH HHS/ -- AI102942/AI/NIAID NIH HHS/ -- AI106697/AI/NIAID NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- F32-AI085828/AI/NIAID NIH HHS/ -- HHSN272201300006C/PHS HHS/ -- K08 DK097301/DK/NIDDK NIH HHS/ -- K08-DK097301/DK/NIDDK NIH HHS/ -- MR/J001929/1/Medical Research Council/United Kingdom -- P01 AI106697/AI/NIAID NIH HHS/ -- P30-AI045008/AI/NIAID NIH HHS/ -- P30-DK050306/DK/NIDDK NIH HHS/ -- R01 AI 084887/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI097333/AI/NIAID NIH HHS/ -- R01 AI102942/AI/NIAID NIH HHS/ -- R21 AI087990/AI/NIAID NIH HHS/ -- T32-AI007532/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Universite Paris Descartes, Paris, France. ; Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/immunology ; Caliciviridae Infections/*immunology ; Coinfection/*immunology/microbiology/parasitology ; Gastroenteritis/*immunology/virology ; Germ-Free Life ; *Immunomodulation ; Intestines/immunology/microbiology/virology ; Lectins/*immunology ; Macrophage Activation ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Microbiota/*immunology ; Norovirus/*immunology ; Trichinella/*immunology ; Trichinellosis/*immunology ; beta-N-Acetylhexosaminidases/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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