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  • 1
    Publication Date: 2015-11-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenbarth, Stephanie C -- Williams, Adam -- Colegio, Oscar R -- Meng, Hailong -- Strowig, Till -- Rongvaux, Anthony -- Henao-Mejia, Jorge -- Thaiss, Christoph A -- Joly, Sophie -- Gonzalez, David G -- Xu, Lan -- Zenewicz, Lauren A -- Haberman, Ann M -- Elinav, Eran -- Kleinstein, Steven H -- Sutterwala, Fayyaz S -- Flavell, Richard A -- England -- Nature. 2016 Feb 25;530(7591):504. doi: 10.1038/nature16074. Epub 2015 Nov 25.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26605525" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2018-12-11
    Description: We examined the unique contributions of the cytokines IL-21 and IL-4 on germinal center (GC) B cell initiation and subsequent maturation in a murine model system. Similar to other reports, we found T follicular helper cell expression of IL-21 begins prior to T follicular helper cell migration into the B cell follicle and precedes that of IL-4. Consistent with this timing, IL-21 signaling has a greater influence on the perifollicular pre-GC B cell transition to the intrafollicular stage. Notably, Bcl6 hi B cells can form in the combined absence of IL-21R– and STAT6-derived signals; however, these nascent GC B cells cease to proliferate and are more prone to apoptosis. When B cells lack either IL-21R or STAT6, aberrant GCs form atypical centroblasts and centrocytes that differ in their phenotypic maturation and costimulatory molecule expression. Thus, IL-4 and IL-21 play nonredundant roles in the phased progression of GC B cell development that can initiate in the combined absence of these cytokine signals.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 3
    Publication Date: 2012-04-28
    Description: NLRs (nucleotide-binding domain leucine-rich-repeat-containing receptors; NOD-like receptors) are a class of pattern recognition receptor (PRR) that respond to host perturbation from either infectious agents or cellular stress. The function of most NLR family members has not been characterized and their role in instructing adaptive immune responses remains unclear. NLRP10 (also known as PYNOD, NALP10, PAN5 and NOD8) is the only NLR lacking the putative ligand-binding leucine-rich-repeat domain, and has been postulated to be a negative regulator of other NLR members, including NLRP3 (refs 4-6). We did not find evidence that NLRP10 functions through an inflammasome to regulate caspase-1 activity nor that it regulates other inflammasomes. Instead, Nlrp10(-/-) mice had a profound defect in helper T-cell-driven immune responses to a diverse array of adjuvants, including lipopolysaccharide, aluminium hydroxide and complete Freund's adjuvant. Adaptive immunity was impaired in the absence of NLRP10 because of a dendritic cell (DC) intrinsic defect in emigration from inflamed tissues, whereas upregulation of DC costimulatory molecules and chemotaxis to CCR7-dependent and -independent ligands remained intact. The loss of antigen transport to the draining lymph nodes by a subset of migratory DCs resulted in an almost absolute loss in naive CD4(+) T-cell priming, highlighting the critical link between diverse innate immune stimulation, NLRP10 activity and the immune function of mature DCs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3340615/" 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/PMC3340615/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenbarth, Stephanie C -- Williams, Adam -- Colegio, Oscar R -- Meng, Hailong -- Strowig, Till -- Rongvaux, Anthony -- Henao-Mejia, Jorge -- Thaiss, Christoph A -- Joly, Sophie -- Gonzalez, David G -- Xu, Lan -- Zenewicz, Lauren A -- Haberman, Ann M -- Elinav, Eran -- Kleinstein, Steven H -- Sutterwala, Fayyaz S -- Flavell, Richard A -- 1 P50 CA121974/CA/NCI NIH HHS/ -- 5KL2RR024138/RR/NCRR NIH HHS/ -- K08 AI085038/AI/NIAID NIH HHS/ -- K08 AI085038-03/AI/NIAID NIH HHS/ -- K08AI085038/AI/NIAID NIH HHS/ -- P30AR053495/AR/NIAMS NIH HHS/ -- R01 AI087630/AI/NIAID NIH HHS/ -- R01AI087630/AI/NIAID NIH HHS/ -- T32HL007974/HL/NHLBI NIH HHS/ -- UL1 RR024139/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Apr 25;484(7395):510-3. doi: 10.1038/nature11012.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22538615" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity/*immunology ; Adjuvants, Immunologic ; Animals ; Antigens/immunology ; Apoptosis Regulatory Proteins/deficiency/genetics/immunology/*metabolism ; Caspase 1 ; Cell Movement ; Chemokines/immunology ; Dendritic Cells/cytology/*immunology/metabolism ; Gene Deletion ; Inflammasomes ; Ligands ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Vaccines/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-04-08
    Description: Tissue homeostasis is achieved through a balance of cell production (growth) and elimination (regression). In contrast to tissue growth, the cells and molecular signals required for tissue regression remain unknown. To investigate physiological tissue regression, we use the mouse hair follicle, which cycles stereotypically between phases of growth and regression while maintaining a pool of stem cells to perpetuate tissue regeneration. Here we show by intravital microscopy in live mice that the regression phase eliminates the majority of the epithelial cells by two distinct mechanisms: terminal differentiation of suprabasal cells and a spatial gradient of apoptosis of basal cells. Furthermore, we demonstrate that basal epithelial cells collectively act as phagocytes to clear dying epithelial neighbours. Through cellular and genetic ablation we show that epithelial cell death is extrinsically induced through transforming growth factor (TGF)-beta activation and mesenchymal crosstalk. Strikingly, our data show that regression acts to reduce the stem cell pool, as inhibition of regression results in excess basal epithelial cells with regenerative abilities. This study identifies the cellular behaviours and molecular mechanisms of regression that counterbalance growth to maintain tissue homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457634/" 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/PMC4457634/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mesa, Kailin R -- Rompolas, Panteleimon -- Zito, Giovanni -- Myung, Peggy -- Sun, Thomas Y -- Brown, Samara -- Gonzalez, David G -- Blagoev, Krastan B -- Haberman, Ann M -- Greco, Valentina -- 1R01AR063663-01/AR/NIAMS NIH HHS/ -- 2P50CA121974/CA/NCI NIH HHS/ -- 5 P30 AR053495-07/AR/NIAMS NIH HHS/ -- 5T32 GM007223/GM/NIGMS NIH HHS/ -- K08 AR066790/AR/NIAMS NIH HHS/ -- P30 AR053495/AR/NIAMS NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Jun 4;522(7554):94-7. doi: 10.1038/nature14306. Epub 2015 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; Department of Biopathology and Medical Biotechnology, University of Palermo, via Divisi 83, 90100 Palermo, Italy. ; 1] Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA [2] Department of Dermatology, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; Department of Laboratory Medicine, Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06510, USA. ; 1] National Science Foundation, Arlington, Virginia 22230, USA [2] AA Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. ; 1] Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA [2] Department of Dermatology, Yale School of Medicine, New Haven, Connecticut 06510, USA [3] Yale Stem Cell Center, Yale School of Medicine, New Haven, Connecticut 06510, USA [4] Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25849774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *Cell Death ; Dermis/cytology/metabolism ; Epithelial Cells/*cytology/metabolism ; Hair Follicle/*cytology/metabolism ; Homeostasis ; Mice ; Phagocytes/cytology ; *Phagocytosis ; Regeneration ; Signal Transduction ; Stem Cell Niche/*physiology ; Stem Cells/*cytology/metabolism ; Transforming Growth Factor beta/metabolism ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-12-11
    Description: Histone demethylase LSD1 is required for germinal center formation and BCL6-driven lymphomagenesis Histone demethylase LSD1 is required for germinal center formation and BCL6-driven lymphomagenesis, Published online: 10 December 2018; doi:10.1038/s41590-018-0273-1 Germinal center B cells undergo reiterative rounds of proliferation and selection. Melnick and colleagues show that the histone demethylase LSD1 is necessary for this reiterative process via its interactions with the transcription factor BCL6.
    Print ISSN: 1529-2908
    Electronic ISSN: 1529-2916
    Topics: Biology , Medicine
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  • 6
    Publication Date: 2011-07-19
    Description: Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148838/" 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/PMC3148838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esplugues, Enric -- Huber, Samuel -- Gagliani, Nicola -- Hauser, Anja E -- Town, Terrence -- Wan, Yisong Y -- O'Connor, William Jr -- Rongvaux, Anthony -- Van Rooijen, Nico -- Haberman, Ann M -- Iwakura, Yoichiro -- Kuchroo, Vijay K -- Kolls, Jay K -- Bluestone, Jeffrey A -- Herold, Kevan C -- Flavell, Richard A -- DK45735/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-20/DK/NIDDK NIH HHS/ -- R01 HL061271/HL/NHLBI NIH HHS/ -- R01 HL062052/HL/NHLBI NIH HHS/ -- R21 HL104601/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jul 17;475(7357):514-8. doi: 10.1038/nature10228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. enric.esplugues@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21765430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology/pharmacology ; Antigens, CD3/immunology ; CD4-Positive T-Lymphocytes/immunology/transplantation ; Cell Movement/drug effects ; Chemokine CCL20/immunology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Gene Expression Profiling ; Gene Expression Regulation/immunology ; Influenza A virus/immunology ; Interleukin-17/immunology ; Intestine, Small/cytology/*immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Orthomyxoviridae Infections/immunology ; Receptors, CCR6/immunology ; Sepsis/immunology ; Staphylococcal Infections/immunology ; Th17 Cells/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2012-07-06
    Description: Tissue development and regeneration depend on cell-cell interactions and signals that target stem cells and their immediate progeny. However, the cellular behaviours that lead to a properly regenerated tissue are not well understood. Using a new, non-invasive, intravital two-photon imaging approach we study physiological hair-follicle regeneration over time in live mice. By these means we have monitored the behaviour of epithelial stem cells and their progeny during physiological hair regeneration and addressed how the mesenchyme influences their behaviour. Consistent with earlier studies, stem cells are quiescent during the initial stages of hair regeneration, whereas the progeny are more actively dividing. Moreover, stem cell progeny divisions are spatially organized within follicles. In addition to cell divisions, coordinated cell movements of the progeny allow the rapid expansion of the hair follicle. Finally, we show the requirement of the mesenchyme for hair regeneration through targeted cell ablation and long-term tracking of live hair follicles. Thus, we have established an in vivo approach that has led to the direct observation of cellular mechanisms of growth regulation within the hair follicle and that has enabled us to precisely investigate functional requirements of hair-follicle components during the process of physiological regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772651/" 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/PMC3772651/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rompolas, Panteleimon -- Deschene, Elizabeth R -- Zito, Giovanni -- Gonzalez, David G -- Saotome, Ichiko -- Haberman, Ann M -- Greco, Valentina -- P30 AR053495/AR/NIAMS NIH HHS/ -- P30AR053495/AR/NIAMS NIH HHS/ -- R01 AR063663/AR/NIAMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Jul 26;487(7408):496-9. doi: 10.1038/nature11218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Movement ; Cell Survival ; Cell Tracking ; Dermis/cytology ; Hair Follicle/*cytology ; Laser Therapy ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence, Multiphoton ; Regeneration/*physiology ; Stem Cells/*cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2013-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolukbasi, Burcu -- Berente, Nicholas -- Cutcher-Gershenfeld, Joel -- Dechurch, Leslie -- Flint, Courtney -- Haberman, Michael -- King, John Leslie -- Knight, Eric -- Lawrence, Barbara -- Masella, Ethan -- McElroy, Charles -- Mittleman, Barbara -- Nolan, Mark -- Radik, Melanie -- Shin, Namchul -- Thompson, Cheryl A -- Winter, Susan -- Zaslavsky, Ilya -- Allison, M Lee -- Arctur, David -- Arrigo, Jennifer -- Aufdenkampe, Anthony K -- Bass, Jay -- Crowell, Jim -- Daniels, Mike -- Diggs, Stephen -- Duffy, Christopher -- Gil, Yolanda -- Gomez, Basil -- Graves, Sara -- Hazen, Robert -- Hsu, Leslie -- Kinkade, Danie -- Lehnert, Kerstin -- Marone, Chris -- Middleton, Don -- Noren, Anders -- Pearthree, Genevieve -- Ramamurthy, Mohan -- Robinson, Erin -- Percivall, George -- Richard, Stephen -- Suarez, Celina -- Walker, Doug -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1041-2. doi: 10.1126/science.342.6162.1041-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Labor and Employment Relations, University of Illinois at Urbana-Champaign, Champaign, IL 61820, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288316" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Periodicals as Topic/*economics ; Research/*economics
    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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  • 9
    ISSN: 1434-6052
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract A permutationally-symmetric form for the nucleon wave function consisting of a linear combination of the56 ground state and the70 excited state is used to reexamine the nucleon structure functions and form factors. This form of wave function reproduces the results of the successful Carlitz-Kaur model, differing only in the addition of a term that is proportional to the square of the mixing coefficient between the56 and the70 states. Values of this mixing coefficient are obtained from the structure functions and from the initial slope of the neutron electric form factor using relativistic wave functions constructed by Henriques, Kellett, and Moorhouse. The signs of these values are in agreement, so that the model avoids the contradiction noted by Le Yaouanc et al. This result is due to the dependence of the neutron electric form factor calculation on the spin wave function and associated matrix elements.
    Type of Medium: Electronic Resource
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