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  • 1
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    Phosphatidylserine receptor is required for clearance of apoptotic cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: Cells undergoing apoptosis during development are removed by phagocytes, but the underlying mechanisms of this process are not fully understood. Phagocytes lacking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells. Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing abnormal development and leading to neonatal lethality. A fraction of PSR knockout mice manifested a hyperplasic brain phenotype resembling that of mice deficient in the cell death-associated genes encoding Apaf-1, caspase-3, and caspase-9, which suggests that phagocytes may also be involved in promoting apoptosis. These data demonstrate a critical role for PSR in early stages of mammalian organogenesis and suggest that this receptor may be involved in respiratory distress syndromes and congenital brain malformations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Ming O -- Sarkisian, Matthew R -- Mehal, Wajahat Z -- Rakic, Pasko -- Flavell, Richard A -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/abnormalities/cytology/*embryology ; Cell Division ; Cell Nucleus/ultrastructure ; Epithelial Cells/physiology/ultrastructure ; Eye/embryology ; Eye Abnormalities/etiology ; Hematopoietic Stem Cell Transplantation ; In Situ Nick-End Labeling ; Inflammation ; Lung/cytology/*embryology/physiology ; Macrophages/*physiology ; Mesoderm/ultrastructure ; Mice ; Mice, Knockout ; Necrosis ; Neurons/cytology ; Phagocytosis ; Phenotype ; Phosphatidylserines/metabolism ; Pulmonary Surfactants/metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Respiratory Insufficiency/etiology ; Reverse Transcriptase Polymerase Chain Reaction
    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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    Novel Foxo1-dependent transcriptional programs control T(reg) cell function (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-11-09
    Description: Regulatory T (T(reg)) cells, characterized by expression of the transcription factor forkhead box P3 (Foxp3), maintain immune homeostasis by suppressing self-destructive immune responses. Foxp3 operates as a late-acting differentiation factor controlling T(reg) cell homeostasis and function, whereas the early T(reg)-cell-lineage commitment is regulated by the Akt kinase and the forkhead box O (Foxo) family of transcription factors. However, whether Foxo proteins act beyond the T(reg)-cell-commitment stage to control T(reg) cell homeostasis and function remains largely unexplored. Here we show that Foxo1 is a pivotal regulator of T(reg )cell function. T(reg) cells express high amounts of Foxo1 and display reduced T-cell-receptor-induced Akt activation, Foxo1 phosphorylation and Foxo1 nuclear exclusion. Mice with T(reg)-cell-specific deletion of Foxo1 develop a fatal inflammatory disorder similar in severity to that seen in Foxp3-deficient mice, but without the loss of T(reg) cells. Genome-wide analysis of Foxo1 binding sites reveals ~300 Foxo1-bound target genes, including the pro-inflammatory cytokine Ifng, that do not seem to be directly regulated by Foxp3. These findings show that the evolutionarily ancient Akt-Foxo1 signalling module controls a novel genetic program indispensable for T(reg) cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771531/" 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/PMC3771531/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouyang, Weiming -- Liao, Will -- Luo, Chong T -- Yin, Na -- Huse, Morgan -- Kim, Myoungjoo V -- Peng, Min -- Chan, Pamela -- Ma, Qian -- Mo, Yifan -- Meijer, Dies -- Zhao, Keji -- Rudensky, Alexander Y -- Atwal, Gurinder -- Zhang, Michael Q -- Li, Ming O -- HG001696/HG/NHGRI NIH HHS/ -- R01 HG001696/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 22;491(7425):554-9. doi: 10.1038/nature11581. Epub 2012 Nov 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Nucleus/metabolism/pathology ; Female ; Forkhead Transcription Factors/*metabolism ; Gene Expression Regulation/genetics ; Genome/genetics ; Immune Tolerance/genetics/immunology ; Interferon-gamma/deficiency/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes, Regulatory/*immunology/*metabolism/pathology ; *Transcription, Genetic
    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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    The cellular and molecular origin of tumor-associated macrophages (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-09
    Description: Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases, including cancer. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). TAMs express the adhesion molecule Vcam1 and proliferate upon their differentiation from inflammatory monocytes, but do not exhibit an "alternatively activated" phenotype. TAM terminal differentiation depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204732/" 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/PMC4204732/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franklin, Ruth A -- Liao, Will -- Sarkar, Abira -- Kim, Myoungjoo V -- Bivona, Michael R -- Liu, Kang -- Pamer, Eric G -- Li, Ming O -- AI101251/AI/NIAID NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 AI101251/AI/NIAID NIH HHS/ -- R37 AI039031/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 May 23;344(6186):921-5. doi: 10.1126/science.1252510. Epub 2014 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA. ; New York Genome Center, New York, NY 10022, USA. ; Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. ; Department of Microbiology and Immunology, Columbia University, New York, NY 10032, USA. ; Immunology Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. lim@mskcc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line, Tumor ; Cell Proliferation ; Female ; Inflammation/immunology/pathology ; Macrophages/*immunology ; Mammary Neoplasms, Animal/*immunology/*pathology ; Mice ; Mice, Inbred C57BL ; Monocyte-Macrophage Precursor Cells/immunology ; Receptors, Notch/metabolism ; Signal Transduction ; Vascular Cell Adhesion Molecule-1/metabolism
    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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    Graded Foxo1 activity in Treg cells differentiates tumour immunity from spontaneous autoimmunity (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-21
    Description: Regulatory T (Treg) cells expressing the transcription factor Foxp3 have a pivotal role in maintaining immunological self-tolerance; yet, excessive Treg cell activities suppress anti-tumour immune responses. Compared to the resting Treg (rTreg) cell phenotype in secondary lymphoid organs, Treg cells in non-lymphoid tissues exhibit an activated Treg (aTreg) cell phenotype. However, the function of aTreg cells and whether their generation can be manipulated are largely unexplored. Here we show that the transcription factor Foxo1, previously demonstrated to promote Treg cell suppression of lymphoproliferative diseases, has an unexpected function in inhibiting aTreg-cell-mediated immune tolerance in mice. We find that aTreg cells turned over at a slower rate than rTreg cells, but were not locally maintained in tissues. aTreg cell differentiation was associated with repression of Foxo1-dependent gene transcription, concomitant with reduced Foxo1 expression, cytoplasmic localization and enhanced phosphorylation at the Akt sites. Treg-cell-specific expression of an Akt-insensitive Foxo1 mutant prevented downregulation of lymphoid organ homing molecules, and impeded Treg cell homing to non-lymphoid organs, causing CD8(+) T-cell-mediated autoimmune diseases. Compared to Treg cells from healthy tissues, tumour-infiltrating Treg cells downregulated Foxo1 target genes more substantially. Expression of the Foxo1 mutant at a lower dose was sufficient to deplete tumour-associated Treg cells, activate effector CD8(+) T cells, and inhibit tumour growth without inflicting autoimmunity. Thus, Foxo1 inactivation is essential for the migration of aTreg cells that have a crucial function in suppressing CD8(+) T-cell responses; and the Foxo signalling pathway in Treg cells can be titrated to break tumour immune tolerance preferentially.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luo, Chong T -- Liao, Will -- Dadi, Saida -- Toure, Ahmed -- Li, Ming O -- P30 CA008748/CA/NCI NIH HHS/ -- R01 AI102888-01A1/AI/NIAID NIH HHS/ -- England -- Nature. 2016 Jan 28;529(7587):532-6. doi: 10.1038/nature16486. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Louis V. Gerstner Jr Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; New York Genome Center, New York, New York 10013, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789248" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Differentiation ; Cell Movement/immunology ; Down-Regulation ; Female ; Forkhead Transcription Factors/biosynthesis/genetics/*metabolism ; Immune Tolerance/*immunology ; Lymphocyte Activation ; Lymphocytes, Tumor-Infiltrating/cytology/immunology/metabolism ; Male ; Mice ; Mutation ; Neoplasms/*immunology ; Phosphorylation ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/cytology/*immunology/*metabolism ; Transcription, Genetic
    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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    Autocrine/paracrine TGF- 1 inhibits Langerhans cell migration (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-11
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    TGF-  regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-03-18
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    The stumpy gene is required for mammalian ciliogenesis (2008)
    National Academy of Sciences
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    Publication Date: 2008-02-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Notch ligand Dll1 mediates cross-talk between mammary stem cells and the macrophageal niche (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-06-29
    Description: The stem cell niche is a specialized environment that dictates stem cell function during development and homeostasis. We show that Dll1, a Notch pathway ligand, is enriched in mammary gland stem cells (MaSCs) and mediates critical interactions with stromal macrophages in the surrounding niche in mouse models. Conditional deletion of Dll1 reduced the number of MaSCs and impaired ductal morphogenesis in the mammary gland. Moreover, MaSC-expressed Dll1 activates Notch signaling in stromal macrophages, increasing their expression of Wnt family ligands such as Wnt3, Wnt10A, and Wnt16, thereby initiating a feedback loop that promotes the function of Dll1-expressing MaSCs. Together, these findings reveal functionally important cross-talk between MaSCs and their macrophageal niche through Dll1-mediated Notch signaling.
    Keywords: Development, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    TGF-{beta} inhibits LC migration [Immunology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-27
    Description: Langerhans cells (LCs) are skin-resident dendritic cells (DC) located in the epidermis that migrate to skin-draining lymph nodes during the steady state and in response to inflammatory stimuli. TGF-β1 is a critical immune regulator that is highly expressed by LCs. The ability to test the functional importance of LC-derived TGF-β1 is complicated by the requirement of TGF-β1 for LC development and by the absence of LCs in mice with an LC-specific ablation of TGF-β1 or its receptor. To overcome these problems, we have engineered transgenic huLangerin-CreERT2 mice that allow for inducible LC-specific excision. Highly efficient and LC-specific expression was confirmed in mice bred onto a YFP Cre reporter strain. We next generated huLangerin-CreERT2 × TGF-βRIIfl and huLangerin-CreERT2 × TGF-β1fl mice. Excision of the TGFβRII or TGFβ1 genes induced mass migration of LCs to the regional lymph node. Expression of costimulatory markers and inflammatory cytokines was unaffected, consistent with homeostatic migration. In addition, levels of p-SMAD2/3 were decreased in LCs from wild-type mice before inflammation-induced migration. We conclude that TGF-β1 acts directly on LCs in an autocrine/paracrine manner to inhibit steady-state and inflammation-induced migration. This is a readily targetable pathway with potential therapeutic implications for skin disease.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Aerobic glycolysis promotes T helper 1 cell differentiation through an epigenetic mechanism (2016)
    American Association for the Advancement of Science
    Details
    Publication Date: 2016-09-29
    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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