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  • 1
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    Intestinal inflammation despite B7-1/B7-2 deprivation [Immunology and Inflammation] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-07-23
    Description: The costimulatory B7-1 (CD80)/B7-2 (CD86) molecules, along with T-cell receptor stimulation, together facilitate T-cell activation. This explains why in vivo B7 costimulation neutralization efficiently silences a variety of human autoimmune disorders. Paradoxically, however, B7 blockade also potently moderates accumulation of immune-suppressive regulatory T cells (Tregs) essential for protection against multiorgan...
    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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  • 2
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    Proteolytic elimination of N-myristoyl modifications by the Shigella virulence factor IpaJ (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-29
    Description: Protein N-myristoylation is a 14-carbon fatty-acid modification that is conserved across eukaryotic species and occurs on nearly 1% of the cellular proteome. The ability of the myristoyl group to facilitate dynamic protein-protein and protein-membrane interactions (known as the myristoyl switch) makes it an essential feature of many signal transduction systems. Thus pathogenic strategies that facilitate protein demyristoylation would markedly alter the signalling landscape of infected host cells. Here we describe an irreversible mechanism of protein demyristoylation catalysed by invasion plasmid antigen J (IpaJ), a previously uncharacterized Shigella flexneri type III effector protein with cysteine protease activity. A yeast genetic screen for IpaJ substrates identified ADP-ribosylation factor (ARF)1p and ARF2p, small molecular mass GTPases that regulate cargo transport through the Golgi apparatus. Mass spectrometry showed that IpaJ cleaved the peptide bond between N-myristoylated glycine-2 and asparagine-3 of human ARF1, thereby providing a new mechanism for host secretory inhibition by a bacterial pathogen. We further demonstrate that IpaJ cleaves an array of N-myristoylated proteins involved in cellular growth, signal transduction, autophagasome maturation and organelle function. Taken together, these findings show a previously unrecognized pathogenic mechanism for the site-specific elimination of N-myristoyl protein modification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722872/" 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/PMC3722872/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnaevskiy, Nikolay -- Fox, Thomas G -- Plymire, Daniel A -- Ertelt, James M -- Weigele, Bethany A -- Selyunin, Andrey S -- Way, Sing Sing -- Patrie, Steven M -- Alto, Neal M -- 5T32AI007520/AI/NIAID NIH HHS/ -- R01 AI083359/AI/NIAID NIH HHS/ -- R01 AI087830/AI/NIAID NIH HHS/ -- R01 AI100934/AI/NIAID NIH HHS/ -- R01 GM100486/GM/NIGMS NIH HHS/ -- R01AI083359/AI/NIAID NIH HHS/ -- R01GM100486/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 4;496(7443):106-9. doi: 10.1038/nature12004. Epub 2013 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8816, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23535599" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/chemistry/metabolism ; ADP-Ribosylation Factors/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Bacterial/*metabolism ; Asparagine/metabolism ; Autophagy ; Biocatalysis ; Cysteine Proteases/metabolism ; Dysentery, Bacillary ; Female ; Glycine/metabolism ; Golgi Apparatus/metabolism/pathology ; HEK293 Cells ; HeLa Cells ; Humans ; Listeria monocytogenes/physiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myristic Acid/*metabolism ; Phagosomes/metabolism ; *Protein Processing, Post-Translational ; *Proteolysis ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae Proteins/metabolism ; Sequence Alignment ; Shigella flexneri/enzymology/*metabolism ; Signal Transduction ; Substrate Specificity ; Virulence ; Virulence Factors/*metabolism
    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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    Pregnancy imprints regulatory memory that sustains anergy to fetal antigen (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-02
    Description: Pregnancy is an intricately orchestrated process where immune effector cells with fetal specificity are selectively silenced. This requires the sustained expansion of immune-suppressive maternal FOXP3(+) regulatory T cells (T(reg) cells), because even transient partial ablation triggers fetal-specific effector T-cell activation and pregnancy loss. In turn, many idiopathic pregnancy complications proposed to originate from disrupted fetal tolerance are associated with blunted maternal T(reg) expansion. Importantly, however, the antigen specificity and cellular origin of maternal T(reg) cells that accumulate during gestation remain incompletely defined. Here we show that pregnancy selectively stimulates the accumulation of maternal FOXP3(+) CD4 cells with fetal specificity using tetramer-based enrichment that allows the identification of rare endogenous T cells. Interestingly, after delivery, fetal-specific T(reg) cells persist at elevated levels, maintain tolerance to pre-existing fetal antigen, and rapidly re-accumulate during subsequent pregnancy. The accelerated expansion of T(reg) cells during secondary pregnancy was driven almost exclusively by proliferation of fetal-specific FOXP3(+) cells retained from prior pregnancy, whereas induced FOXP3 expression and proliferation of pre-existing FOXP3(+) cells each contribute to T(reg) expansion during primary pregnancy. Furthermore, fetal resorption in secondary compared with primary pregnancy becomes more resilient to partial maternal FOXP3(+) cell ablation. Thus, pregnancy imprints FOXP3(+) CD4 cells that sustain protective regulatory memory to fetal antigen. We anticipate that these findings will spark further investigation on maternal regulatory T-cell specificity that unlocks new strategies for improving pregnancy outcomes and novel approaches for therapeutically exploiting T(reg) cell memory.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3465465/" 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/PMC3465465/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowe, Jared H -- Ertelt, James M -- Xin, Lijun -- Way, Sing Sing -- F30 DK084674/DK/NIDDK NIH HHS/ -- F30DK084674/DK/NIDDK NIH HHS/ -- R01 AI087830/AI/NIAID NIH HHS/ -- R01 AI100934/AI/NIAID NIH HHS/ -- R01AI087830/AI/NIAID NIH HHS/ -- R01AI100934/AI/NIAID NIH HHS/ -- England -- Nature. 2012 Oct 4;490(7418):102-6. doi: 10.1038/nature11462. Epub 2012 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Minnesota School of Medicine, Department of Pediatrics, Minneapolis, Minnesota 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23023128" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigens/*immunology ; CD4-Positive T-Lymphocytes/cytology/immunology/metabolism/transplantation ; Clonal Anergy/*immunology ; Female ; Fetal Proteins/*immunology ; Fetus/immunology ; Forkhead Transcription Factors/metabolism ; Immunologic Memory/genetics/*immunology ; Interferon-gamma/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Postpartum Period/immunology ; Pregnancy ; T-Lymphocytes, Regulatory/cytology/immunology/metabolism
    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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    Immunosuppressive CD71+ erythroid cells compromise neonatal host defence against infection (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-11-08
    Description: Newborn infants are highly susceptible to infection. This defect in host defence has generally been ascribed to the immaturity of neonatal immune cells; however, the degree of hyporesponsiveness is highly variable and depends on the stimulation conditions. These discordant responses illustrate the need for a more unified explanation for why immunity is compromised in neonates. Here we show that physiologically enriched CD71(+) erythroid cells in neonatal mice and human cord blood have distinctive immunosuppressive properties. The production of innate immune protective cytokines by adult cells is diminished after transfer to neonatal mice or after co-culture with neonatal splenocytes. Neonatal CD71(+) cells express the enzyme arginase-2, and arginase activity is essential for the immunosuppressive properties of these cells because molecular inhibition of this enzyme or supplementation with L-arginine overrides immunosuppression. In addition, the ablation of CD71(+) cells in neonatal mice, or the decline in number of these cells as postnatal development progresses parallels the loss of suppression, and restored resistance to the perinatal pathogens Listeria monocytogenes and Escherichia coli. However, CD71(+) cell-mediated susceptibility to infection is counterbalanced by CD71(+) cell-mediated protection against aberrant immune cell activation in the intestine, where colonization with commensal microorganisms occurs swiftly after parturition. Conversely, circumventing such colonization by using antimicrobials or gnotobiotic germ-free mice overrides these protective benefits. Thus, CD71(+) cells quench the excessive inflammation induced by abrupt colonization with commensal microorganisms after parturition. This finding challenges the idea that the susceptibility of neonates to infection reflects immune-cell-intrinsic defects and instead highlights processes that are developmentally more essential and inadvertently mitigate innate immune protection. We anticipate that these results will spark renewed investigation into the need for immunosuppression in neonates, as well as improved strategies for augmenting host defence in this vulnerable population.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3979598/" 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/PMC3979598/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elahi, Shokrollah -- Ertelt, James M -- Kinder, Jeremy M -- Jiang, Tony T -- Zhang, Xuzhe -- Xin, Lijun -- Chaturvedi, Vandana -- Strong, Beverly S -- Qualls, Joseph E -- Steinbrecher, Kris A -- Kalfa, Theodosia A -- Shaaban, Aimen F -- Way, Sing Sing -- P30 DK090971/DK/NIDDK NIH HHS/ -- R01 AI087830/AI/NIAID NIH HHS/ -- R01 AI100934/AI/NIAID NIH HHS/ -- R01 HL103745/HL/NHLBI NIH HHS/ -- R01 HL116352/HL/NHLBI NIH HHS/ -- R01AI087830/AI/NIAID NIH HHS/ -- R01AI100934/AI/NIAID NIH HHS/ -- R01HL103745/HL/NHLBI NIH HHS/ -- R21 AI107274/AI/NIAID NIH HHS/ -- T32 GM063483/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Dec 5;504(7478):158-62. doi: 10.1038/nature12675. Epub 2013 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24196717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigens, CD/*metabolism ; Arginase/genetics/metabolism ; Disease Susceptibility/immunology ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Erythroid Cells/enzymology/*immunology ; Escherichia coli/immunology ; Escherichia coli Infections/*immunology ; Female ; Fetal Blood/cytology ; Humans ; Immune Tolerance/drug effects/genetics/*immunology ; Listeria monocytogenes/immunology ; Listeriosis/*immunology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Transferrin/*metabolism ; Tumor Necrosis Factor-alpha/metabolism
    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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    Nonrandom attrition of the naive CD8+ T-cell pool with aging governed by T-cell receptor:pMHC interactions (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-08-03
    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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    Commensal microbes drive intestinal inflammation by IL-17-producing CD4+ T cells through ICOSL and OX40L costimulation in the absence of B7-1 and B7-2 (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-07-07
    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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    Nonrandom attrition of the naive CD8+ T-cell pool with aging governed by T-cell receptor:pMHC interactions [Immunology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-08-18
    Description: Immunity against new infections declines in the last quartile of life, as do numbers of naive T cells. Peripheral maintenance of naive T cells over the lifespan is necessary because their production drastically declines by puberty, a result of thymic involution. We report that this maintenance is not random in advanced aging. As numbers and diversity of naive CD8+ T cells declined with aging, surviving cells underwent faster rates of homeostatic proliferation, were selected for high T-cell receptor:pMHC avidity, and preferentially acquired “memory-like” phenotype. These high-avidity precursors preferentially responded to infection and exhibited strong antimicrobial function. Thus, T-cell receptor avidity for self-pMHC provides a proofreading mechanism to maintain some of the fittest T cells in the otherwise crumbling naive repertoire, providing a degree of compensation for numerical and diversity defects in old T cells.
    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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