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  • 1
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    Requirement for RORgamma in thymocyte survival and lymphoid organ development (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
    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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    TGF-beta-induced Foxp3 inhibits T(H)17 cell differentiation by antagonizing RORgammat function (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-28
    Description: T helper cells that produce IL-17 (T(H)17 cells) promote autoimmunity in mice and have been implicated in the pathogenesis of human inflammatory diseases. At mucosal surfaces, T(H)17 cells are thought to protect the host from infection, whereas regulatory T (T(reg)) cells control immune responses and inflammation triggered by the resident microflora. Differentiation of both cell types requires transforming growth factor-beta (TGF-beta), but depends on distinct transcription factors: RORgammat (encoded by Rorc(gammat)) for T(H)17 cells and Foxp3 for T(reg) cells. How TGF-beta regulates the differentiation of T cells with opposing activities has been perplexing. Here we demonstrate that, together with pro-inflammatory cytokines, TGF-beta orchestrates T(H)17 cell differentiation in a concentration-dependent manner. At low concentrations, TGF-beta synergizes with interleukin (IL)-6 and IL-21 (refs 9-11) to promote IL-23 receptor (Il23r) expression, favouring T(H)17 cell differentiation. High concentrations of TGF-beta repress IL23r expression and favour Foxp3+ T(reg) cells. RORgammat and Foxp3 are co-expressed in naive CD4+ T cells exposed to TGF-beta and in a subset of T cells in the small intestinal lamina propria of the mouse. In vitro, TGF-beta-induced Foxp3 inhibits RORgammat function, at least in part through their interaction. Accordingly, lamina propria T cells that co-express both transcription factors produce less IL-17 (also known as IL-17a) than those that express RORgammat alone. IL-6, IL-21 and IL-23 relieve Foxp3-mediated inhibition of RORgammat, thereby promoting T(H)17 cell differentiation. Therefore, the decision of antigen-stimulated cells to differentiate into either T(H)17 or T(reg) cells depends on the cytokine-regulated balance of RORgammat and Foxp3.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597437/" 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/PMC2597437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Liang -- Lopes, Jared E -- Chong, Mark M W -- Ivanov, Ivaylo I -- Min, Roy -- Victora, Gabriel D -- Shen, Yuelei -- Du, Jianguang -- Rubtsov, Yuri P -- Rudensky, Alexander Y -- Ziegler, Steven F -- Littman, Dan R -- AI48779/AI/NIAID NIH HHS/ -- R01 AI048779/AI/NIAID NIH HHS/ -- R01 AI048779-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 May 8;453(7192):236-40. doi: 10.1038/nature06878. Epub 2008 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18368049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; Cells, Cultured ; Forkhead Transcription Factors/genetics/*metabolism ; Gene Expression Regulation/drug effects ; Humans ; Interleukin-17/biosynthesis/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Interleukin/genetics/metabolism ; Receptors, Retinoic Acid/*antagonists & inhibitors/genetics/metabolism ; Receptors, Thyroid Hormone/*antagonists & inhibitors/genetics/metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/*drug effects/metabolism ; Transforming Growth Factor beta/*pharmacology
    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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  • 3
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    Thymic origin of intestinal alphabeta T cells revealed by fate mapping of RORgammat+ cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Intestinal intraepithelial T lymphocytes (IELs) are likely to play a key role in host mucosal immunity and, unlike other T cells, have been proposed to differentiate from local precursors rather than from thymocytes. We show here that IELs expressing the alphabeta T cell receptor are derived from precursors that express RORgammat, an orphan nuclear hormone receptor detected only in immature CD4+CD8+ thymocytes, fetal lymphoid tissue-inducer (LTi) cells, and LTi-like cells in cryptopatches within the adult intestinal lamina propria. Using cell fate mapping, we found that all intestinal alphabeta T cells are progeny of CD4+CD8+ thymocytes, indicating that the adult intestine is not a significant site for alphabeta T cell development. Our results suggest that intestinal RORgammat+ cells are local organizers of mucosal lymphoid tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eberl, Gerard -- Littman, Dan R -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15247480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Cell Lineage ; DNA-Binding Proteins/metabolism ; Hematopoietic Stem Cells/immunology/physiology ; Immunity, Mucosal ; Intestinal Mucosa/cytology/*immunology ; Lymphoid Tissue/embryology/immunology ; Mice ; Mice, Transgenic ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Antigen, T-Cell, alpha-beta/*analysis/genetics ; Receptors, Antigen, T-Cell, gamma-delta/analysis/genetics ; Receptors, Retinoic Acid/genetics/*metabolism ; Receptors, Thyroid Hormone/genetics/*metabolism ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes/cytology/*immunology ; Thymus Gland/cytology/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    DDX5 and its associated lncRNA Rmrp modulate TH17 cell effector functions (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-12-18
    Description: T helper 17 (TH17) lymphocytes protect mucosal barriers from infections, but also contribute to multiple chronic inflammatory diseases. Their differentiation is controlled by RORgammat, a ligand-regulated nuclear receptor. Here we identify the RNA helicase DEAD-box protein 5 (DDX5) as a RORgammat partner that coordinates transcription of selective TH17 genes, and is required for TH17-mediated inflammatory pathologies. Surprisingly, the ability of DDX5 to interact with RORgammat and coactivate its targets depends on intrinsic RNA helicase activity and binding of a conserved nuclear long noncoding RNA (lncRNA), Rmrp, which is mutated in patients with cartilage-hair hypoplasia. A targeted Rmrp gene mutation in mice, corresponding to a gene mutation in cartilage-hair hypoplasia patients, altered lncRNA chromatin occupancy, and reduced the DDX5-RORgammat interaction and RORgammat target gene transcription. Elucidation of the link between Rmrp and the DDX5-RORgammat complex reveals a role for RNA helicases and lncRNAs in tissue-specific transcriptional regulation, and provides new opportunities for therapeutic intervention in TH17-dependent diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762670/" 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/PMC4762670/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Thomas, Benjamin -- Flynn, Ryan A -- Gavzy, Samuel J -- Wu, Lin -- Kim, Sangwon V -- Hall, Jason A -- Miraldi, Emily R -- Ng, Charles P -- Rigo, Frank W -- Meadows, Sarah -- Montoya, Nina R -- Herrera, Natalia G -- Domingos, Ana I -- Rastinejad, Fraydoon -- Myers, Richard M -- Fuller-Pace, Frances V -- Bonneau, Richard -- Chang, Howard Y -- Acuto, Oreste -- Littman, Dan R -- 1F30CA189514-01/CA/NCI NIH HHS/ -- F30 CA189514/CA/NCI NIH HHS/ -- P50 HG007735/HG/NHGRI NIH HHS/ -- P50-HG007735/HG/NHGRI NIH HHS/ -- R01 AI080885/AI/NIAID NIH HHS/ -- R01 AI121436/AI/NIAID NIH HHS/ -- R01 DK103358/DK/NIDDK NIH HHS/ -- R01 HG004361/HG/NHGRI NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- R01DK103358/DK/NIDDK NIH HHS/ -- R01HG004361/HG/NHGRI NIH HHS/ -- T32 AI100853/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 24;528(7583):517-22. doi: 10.1038/nature16193. Epub 2015 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK. ; Center for Personal Dynamic Regulomes, Stanford University, Stanford, California 94305, USA. ; Center for Genomics and Systems Biology, Department of Biology, New York University, New York, New York 10003, USA. ; Courant Institute of Mathematical Sciences, Computer Science Department, New York University, New York, New York 10012, USA. ; Simons Center for Data Analysis, Simons Foundation, New York, New York 10010, USA. ; Isis Pharmaceuticals, Carlsbad, California 92010, USA. ; HudsonAlpha Institute for Biotechnology, Huntsville, Alabama 35806, USA. ; Instituto Gulbenkian de Ciencia, Oeiras 2780-156, Portugal. ; Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida 32827, USA. ; Division of Cancer Research, University of Dundee, Dundee DD1 9SY, UK. ; Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675721" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/genetics/metabolism ; DEAD-box RNA Helicases/genetics/*metabolism ; Female ; Gene Expression Regulation/genetics ; Hair/abnormalities ; Hirschsprung Disease/genetics ; Humans ; Immunologic Deficiency Syndromes/genetics ; Inflammation/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mutation/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Organ Specificity ; Osteochondrodysplasias/congenital/genetics ; Protein Binding ; RNA, Long Noncoding/genetics/*metabolism ; Th17 Cells/*immunology/*metabolism ; Transcription, Genetic/genetics
    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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    Maternal retinoids control type 3 innate lymphoid cells and set the offspring immunity (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-03-29
    Description: The impact of nutritional status during fetal life on the overall health of adults has been recognized; however, dietary effects on the developing immune system are largely unknown. Development of secondary lymphoid organs occurs during embryogenesis and is considered to be developmentally programmed. Secondary lymphoid organ formation depends on a subset of type 3 innate lymphoid cells (ILC3) named lymphoid tissue inducer (LTi) cells. Here we show that mouse fetal ILC3s are controlled by cell-autonomous retinoic acid (RA) signalling in utero, which pre-sets the immune fitness in adulthood. We found that embryonic lymphoid organs contain ILC progenitors that differentiate locally into mature LTi cells. Local LTi cell differentiation was controlled by maternal retinoid intake and fetal RA signalling acting in a haematopoietic cell-autonomous manner. RA controlled LTi cell maturation upstream of the transcription factor RORgammat. Accordingly, enforced expression of Rorgt restored maturation of LTi cells with impaired RA signalling, whereas RA receptors directly regulated the Rorgt locus. Finally, we established that maternal levels of dietary retinoids control the size of secondary lymphoid organs and the efficiency of immune responses in the adult offspring. Our results reveal a molecular link between maternal nutrients and the formation of immune structures required for resistance to infection in the offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van de Pavert, Serge A -- Ferreira, Manuela -- Domingues, Rita G -- Ribeiro, Helder -- Molenaar, Rosalie -- Moreira-Santos, Lara -- Almeida, Francisca F -- Ibiza, Sales -- Barbosa, Ines -- Goverse, Gera -- Labao-Almeida, Carlos -- Godinho-Silva, Cristina -- Konijn, Tanja -- Schooneman, Dennis -- O'Toole, Tom -- Mizee, Mark R -- Habani, Yasmin -- Haak, Esther -- Santori, Fabio R -- Littman, Dan R -- Schulte-Merker, Stefan -- Dzierzak, Elaine -- Simas, J Pedro -- Mebius, Reina E -- Veiga-Fernandes, Henrique -- R01 AI080885/AI/NIAID NIH HHS/ -- R01AI080885/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Apr 3;508(7494):123-7. doi: 10.1038/nature13158. Epub 2014 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2] Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. [3]. ; 1] Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal [2]. ; Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Av. Prof. Egas Moniz, Edificio Egas Moniz, 1649-028 Lisboa, Portugal. ; Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands. ; Erasmus Stem Cell Institute, Department of Cell Biology, Erasmus Medical Center, 3000 CA Rotterdam, The Netherlands. ; Howard Hughes Medical Institute, Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA. ; Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, 3584 CT Utrecht, Netherlands. ; 1] Department of Molecular Cell Biology and Immunology, VU University Medical Center, van der Boechorststraat 7, 1081BT Amsterdam, The Netherlands [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects/immunology ; Diet ; Female ; Fetus/drug effects/*immunology ; Immunity, Innate/drug effects/*immunology ; Lymphoid Tissue/cytology/drug effects/embryology/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology ; Receptors, Retinoic Acid/metabolism ; Signal Transduction/drug effects ; Stem Cells/cytology/drug effects/immunology ; Tretinoin/administration & dosage/*immunology/metabolism/*pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    A subset of CD4+ thymocytes selected by MHC class I molecules (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: To complete their maturation, most immature thymocytes depend on the simultaneous engagement of their antigen receptor [alpha beta T cell receptor (TCR)] and their CD4 or CD8 coreceptors with major histocompatibility complex class II or I ligands, respectively. However, a normal subset of mature alpha beta TCR+ thymocytes did not follow these rules. These thymocytes expressed NK1.1 and a restricted set of alpha beta TCRs that are intrinsically class I-reactive because their positive selection was class I-dependent but CD8-independent. These cells were CD4+ and CD4-8- but never CD8+, because the presence of CD8 caused negative selection. Thus, neither CD4 nor CD8 contributes signals that direct their maturation into the CD4+ and CD4-8- lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bendelac, A -- Killeen, N -- Littman, D R -- Schwartz, R H -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1774-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Antigens, Ly ; Antigens, Surface ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Female ; Histocompatibility Antigens Class I/*physiology ; Lectins, C-Type ; Ligands ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; NK Cell Lectin-Like Receptor Subfamily B ; Phenotype ; Proteins/analysis ; Receptors, Antigen, T-Cell, alpha-beta/analysis/*physiology ; T-Lymphocyte Subsets/cytology/*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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