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Author Mazzolari, E.; Forino, C.; Fontana, M.; D'Ippolito, C.; Lanfranchi, A.; Gambineri, E.; Ochs, H.; Badolato, R.; Notarangelo, L.D. url  openurl
  Title A new case of IPEX receiving bone marrow transplantation Type Journal Article
  Year 2005 Publication Bone Marrow Transplant Abbreviated Journal  
  Volume 35 Issue 10 Pages 1033-1034  
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  Notes Approved no  
  Call Number MRC @ kga @ Mazzolari2005 Serial 42  
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Author Luo, Z.-X.; Chen, P.; Li, G.; Chen, M. doi  openurl
  Title A new eutriconodont mammal and evolutionary development in early mammals Type Journal Article
  Year 2007 Publication Nature Abbreviated Journal  
  Volume 446 Issue 7133 Pages 288-293  
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  Abstract Detachment of the three tiny middle ear bones from the reptilian mandible is an important innovation of modern mammals. Here we describe a Mesozoic eutriconodont nested within crown mammals that clearly illustrates this transition: the middle ear bones are connected to the mandible via an ossified Meckel's cartilage. The connected ear and jaw structure is similar to the embryonic pattern in modern monotremes (egg-laying mammals) and placental mammals, but is a paedomorphic feature retained in the adult, unlike in monotreme and placental adults. This suggests that reversal to (or retention of) this premammalian ancestral condition is correlated with different developmental timing (heterochrony) in eutriconodonts. This new eutriconodont adds to the evidence of homoplasy of vertebral characters in the thoraco-lumbar transition and unfused lumbar ribs among early mammals. This is similar to the effect of homeobox gene patterning of vertebrae in modern mammals, making it plausible to extrapolate the effects of Hox gene patterning to account for homoplastic evolution of vertebral characters in early mammals.  
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  ISSN 0028-0836 ISBN Medium  
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  Notes 10.1038/nature05627 Approved no  
  Call Number MRC @ kga @ Luo2007 Serial 43  
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Author Vacchio, M.S.; Williams, J.A.; Hodes, R.J. url  openurl
  Title A novel role for CD28 in thymic selection: elimination of CD28/B7 interactions increases positive selection Type Journal Article
  Year 2005 Publication Eur J Immunol Abbreviated Journal  
  Volume 35 Issue 2 Pages 418-427  
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  Abstract While the importance of the CD28/B7 costimulation pathway is well established for mature T cells, the role of CD28 in thymocyte selection is less well defined. The role of CD28 in both negative and positive selection was assessed using H-Y-specific TCR-transgenic (Tg) RAG-2-deficient (H-Yrag) mice. Negative selection in male H-Yrag mice was not affected by deficiency in CD28 or B7. Surprisingly, absence of CD28 or B7 in H-Yrag females resulted in increased numbers of CD8 single-positive (SP) thymocytes. The CD8 SP thymocytes found in these females were mature and functionally competent. Furthermore, double-positive (DP) thymocytes from CD28-knockout (CD28KO) or B7.1/B7.2 double-KO (B7DKO) females had higher levels of both CD5 and TCR than those from WT females, consistent with a stronger selecting signal. CD28KO H-Yrag fetal thymic organ cultures also had elevated numbers of thymic CD8 SP cells, reflecting increased thymic differentiation and not recirculation of peripheral T cells. Finally, increased selection of mature CD4 and CD8 SP T cells was observed in non-TCR-Tg CD28KO and B7DKO mice, indicating that this function of CD28-B7 interaction is not unique to a TCR-Tg model. Together these findings demonstrate a novel negative regulatory role for CD28 in inhibiting differentiation of SP thymocytes, probably through inhibition of thymic selection.  
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  Publisher Place of Publication Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Editor  
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  Notes Approved no  
  Call Number MRC @ kga @ Vacchio2005 Serial 44  
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Author Szabo, S.J.; Kim, S.T.; Costa, G.L.; Zhang, X.; Fathman, C.G.; Glimcher, L.H. url  openurl
  Title A novel transcription factor, T-bet, directs Th1 lineage commitment Type Journal Article
  Year 2000 Publication Cell Abbreviated Journal  
  Volume 100 Issue 6 Pages 655-669  
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  Abstract Naive T helper cells differentiate into two subsets, Th1 and Th2, each with distinct functions and cytokine profiles. Here, we report the isolation of T-bet, a Th1-specific T box transcription factor that controls the expression of the hallmark Th1 cytokine, IFNgamma. T-bet expression correlates with IFNgamma expression in Th1 and NK cells. Ectopic expression of T-bet both transactivates the IFNgamma gene and induces endogenous IFNgamma production. Remarkably, retroviral gene transduction of T-bet into polarized Th2 and Tc2 primary T cells redirects them into Th1 and Tc1 cells, respectively, as evidenced by the simultaneous induction of IFNgamma and repression of IL-4 and IL-5. Thus, T-bet initiates Th1 lineage development from naive Thp cells both by activating Th1 genetic programs and by repressing the opposing Th2 programs.  
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  Publisher Place of Publication Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachus Editor  
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  Call Number MRC @ kga @ Szabo2000 Serial 45  
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Author Li, L.; Iwamoto, Y.; Berezovskaya, A.; Boussiotis, V.A. url  openurl
  Title A pathway regulated by cell cycle inhibitor p27(Kip1) and checkpoint inhibitor Smad3 is involved in the induction of T cell tolerance Type Journal Article
  Year 2006 Publication Nat Immunol Abbreviated Journal  
  Volume 7 Issue 11 Pages 1157-1165  
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  Abstract Peripheral tolerance is essential for immunological homeostasis. Tolerant T cells are thought to arise after T cell receptor ligation in conditions that are nonpermissive for replication. Here we have investigated the function of the cell cycle inhibitor p27(Kip1) in tolerance induction in vivo using naive T cell receptor-transgenic cells lacking the cyclin-dependent kinase (Cdk)-binding domain of p27(Kip1)(p27delta). Wild-type but not p27delta cells underwent tolerization. Tolerized wild-type cells had impaired Cdk2 and Cdc2 kinase activity and failed to phosphorylate the checkpoint inhibitor Smad3, leading to enhanced expression of the Cdk inhibitor p15. In contrast, p27delta cells proliferated in tolerizing conditions because of Cdk kinase activation and phosphorylation of Smad3, which resulted in no upregulation of p15. Smad3 'knockdown' prevented tolerance induction, whereas expression of a Smad3 mutant resistant to Cdk-mediated phosphorylation recapitulated molecular and functional events of tolerance. Thus, p27(Kip1) is required during induction of tolerance and Smad3 regulates T cell responses 'downstream' of p27(Kip1).  
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  Publisher Place of Publication Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Bos Editor  
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  Call Number MRC @ kga @ Li2006 Serial 46  
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Author Benoist, C.; Germain, R.N.; Mathis, D. url  openurl
  Title A plaidoyer for 'systems immunology' Type Journal Article
  Year 2006 Publication Immunol Rev Abbreviated Journal  
  Volume 210 Issue Pages 229-234  
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  Abstract A complete understanding of the immune system will ultimately require an integrated perspective on how genetic and epigenetic entities work together to produce the range of physiologic and pathologic behaviors characteristic of immune function. The immune network encompasses all of the connections and regulatory associations between individual cells and the sum of interactions between gene products within a cell. With 30 000+ protein-coding genes in a mammalian genome, further compounded by microRNAs and yet unrecognized layers of genetic controls, connecting the dots of this network is a monumental task. Over the past few years, high-throughput techniques have allowed a genome-scale view on cell states and cell- or system-level responses to perturbations. Here, we observe that after an early burst of enthusiasm, there has developed a distinct resistance to placing a high value on global genomic or proteomic analyses. Such reluctance has affected both the practice and the publication of immunological science, resulting in a substantial impediment to the advances in our understanding that such large-scale studies could potentially provide. We propose that distinct standards are needed for validation, evaluation, and visualization of global analyses, such that in-depth descriptions of cellular responses may complement the gene/factor-centric approaches currently in favor.  
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  Publisher Place of Publication Section on Immunology and Immunogenetics, Joslin Diabetes Center, Department of Medicine, Brigham an Editor  
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  Notes Approved no  
  Call Number MRC @ kga @ Benoist2006 Serial 47  
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Author Garden, O.A.; Reynolds, P.R.; Yates, J.; Larkman, D.J.; Marelli-Berg, F.M.; Haskard, D.O.; Edwards, A.D.; George, A.J. url  openurl
  Title A rapid method for labelling CD4+ T cells with ultrasmall paramagnetic iron oxide nanoparticles for magnetic resonance imaging that preserves proliferative, regulatory and migratory behaviour in vitro Type Journal Article
  Year 2006 Publication J Immunol Methods Abbreviated Journal  
  Volume 314 Issue 1-2 Pages 123-133  
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  Abstract A number of techniques have been developed to track the migration of T cells in vivo, but they all suffer significant shortcomings, including the examination of selected organs rather than the organism as a whole--thus precluding longitudinal studies--or limitations imposed by poor spatial resolution and the application of ionizing radiation. By conjugating the HIV tat peptide to ultrasmall superparamagnetic iron oxide (USPIO) nanoparticles in a reaction yielding a mean valence of 45, a magnetic resonance (MR) contrast agent was synthesised that allowed T cells to be efficiently labelled within just 5 min. The USPIO nanoparticles were incorporated into both the cytoplasm and nucleus of labelled cells, which retained normal in vitro proliferative responses to a polyclonal stimulus; suppressive responses mediated by labelled CD4(+) CD25(+) regulatory T cells; chemotactic responses to the chemokine CXCL-12; and transmigration of an activated endothelial monolayer. We believe that this rapid, efficient and essentially non-toxic approach to labelling both murine and human T cells for MRI holds considerable promise, paving the way for the wider immunological application of this exciting technology.  
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  Publisher Place of Publication Department of Immunology, Imperial College London, Hammersmith Campus, Du Cane Road, W12 ONN, UK. Editor  
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  Call Number MRC @ kga @ Garden2006 Serial 48  
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Author Bilodeau, M.; Girard, S.; Hebert, J.; Sauvageau, G. url  openurl
  Title A retroviral strategy that efficiently creates chromosomal deletions in mammalian cells Type Journal Article
  Year 2007 Publication Nat Methods Abbreviated Journal  
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  Abstract Chromosomal deletions, as a genetic tool for functional genomics, remain underexploited for vertebrate stem cells mostly because presently available methods are too labor-intensive. To address this, we developed and validated a set of complementary retroviruses that creates a wide range of nested chromosomal deletions. When applied to mouse embryonic stem cells (ESCs), this retrovirus-based method yielded deletions ranging from 6 kb to 23 Mb (average 2.9 Mb), with an efficiency of 64% for drug-selected clones. Notably, several of the engineered ESC clones, mostly those with large deletions, showed major alteration in cell fate. In comparison to other methods that have also exploited retroviruses for chromosomal engineering, this modified strategy is more efficient and versatile because it bypasses the need for homologous recombination, and thus can be exploited for rapid and extensive functional screens in embryonic and adult stem cells.  
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  Publisher Place of Publication Laboratory of Molecular Genetics of Stem Cells, Institute for Research in Immunology and Cancer (IRI Editor  
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  Call Number MRC @ kga @ Bilodeau2007 Serial 49  
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Author Vinuesa, C.G.; Cook, M.C.; Angelucci, C.; Athanasopoulos, V.; Rui, L.; Hill, K.M.; Yu, D.; Domaschenz, H.; Whittle, B.; Lambe, T.; Roberts, I.S.; Copley, R.R.; Bell, J.I.; Cornall, R.J.; Goodnow, C.C. url  openurl
  Title A RING-type ubiquitin ligase family member required to repress follicular helper T cells and autoimmunity Type Journal Article
  Year 2005 Publication Nature Abbreviated Journal  
  Volume 435 Issue 7041 Pages 452-458  
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  Abstract Despite the sequencing of the human and mouse genomes, few genetic mechanisms for protecting against autoimmune disease are currently known. Here we systematically screen the mouse genome for autoimmune regulators to isolate a mouse strain, sanroque, with severe autoimmune disease resulting from a single recessive defect in a previously unknown mechanism for repressing antibody responses to self. The sanroque mutation acts within mature T cells to cause formation of excessive numbers of follicular helper T cells and germinal centres. The mutation disrupts a repressor of ICOS, an essential co-stimulatory receptor for follicular T cells, and results in excessive production of the cytokine interleukin-21. sanroque mice fail to repress diabetes-causing T cells, and develop high titres of autoantibodies and a pattern of pathology consistent with lupus. The causative mutation is in a gene of previously unknown function, roquin (Rc3h1), which encodes a highly conserved member of the RING-type ubiquitin ligase protein family. The Roquin protein is distinguished by the presence of a CCCH zinc-finger found in RNA-binding proteins, and localization to cytosolic RNA granules implicated in regulating messenger RNA translation and stability.  
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  Publisher Place of Publication Division of Immunology and Genetics, John Curtin School of Medical Research, The Australian National Editor  
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  Call Number MRC @ kga @ Vinuesa2005 Serial 50  
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Author Suffia, I.; Reckling, S.K.; Salay, G.; Belkaid, Y. url  openurl
  Title A role for CD103 in the retention of CD4+CD25+ Treg and control of Leishmania major infection Type Journal Article
  Year 2005 Publication J Immunol Abbreviated Journal  
  Volume 174 Issue 9 Pages 5444-5455  
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  Abstract Endogenous regulatory T cells (T(reg)) play a central role in the control of excessive or misdirected immune responses against self or foreign Ags. To date, virtually no data are available on the nature of the molecules and signals involved in the trafficking and retention of T(reg) in tissues where regulation is required. Here, we show that expression of alpha(E)beta(7) integrin is necessary for the homing of T(reg) at site of Leishmania major infection. The vast majority of T(reg) present in the dermis at steady-state conditions or during L. major infection express the alpha(E) chain (CD103) of alpha(E)beta(7). Genetically susceptible BALB/c mice that lack CD103 become resistant to infection, a phenotype that is associated with a poor capacity of T(reg) to be retained in the infected site. Such susceptible phenotype can be restored when T(reg) from wild-type mice were transferred in CD103(-/-) mice. The central role of CD103 in T(reg) retention was further demonstrated by usage of blocking Abs against CD103 and the transfer of T(reg) purified from CD103(-/-) mice. Our results strongly suggest that this molecule is induced and maintained on T(reg) following or just prior to their arrival in tissues. Furthermore, the expression of CD103 and the subsequent retention of T(reg) in tissues is highly regulated by their exposure to Leishmania Ag and the level of activation of the APCs they encounter. Thus, CD103, by controlling T(reg) retention, can contribute to the outcome of chronic infection by Leishmania.  
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  Publisher Place of Publication Division of Molecular Immunology, Cincinnati Children's Hospital Research Foundation, Cincinnati, OH Editor  
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  Notes Approved no  
  Call Number MRC @ kga @ Suffia2005 Serial 51  
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