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Author Bystry, R.S.; Aluvihare, V.; Welch, K.A.; Kallikourdis, M.; Betz, A.G. url  openurl
  Title B cells and professional APCs recruit regulatory T cells via CCL4 Type Journal Article
  Year 2001 Publication Nat Immunol Abbreviated Journal  
  Volume 2 Issue 12 Pages 1126-1132  
  Keywords Animals; Antigen-Presenting Cells/drug effects/*immunology; Autoantibodies/biosynthesis; *Autoimmunity; B-Lymphocytes/*immunology; CD4-Positive T-Lymphocytes/drug effects/*immunology; Cells, Cultured; Chemokines/biosynthesis; *Chemotaxis, Leukocyte; Gene Expression Profiling; Germinal Center/cytology; Immunophenotyping; Lymphocyte Activation; Lymphocyte Depletion; Macrophage Inflammatory Protein-1/pharmacology/*physiology; Mice; RNA, Messenger/biosynthesis; Receptors, Interleukin-2/physiology; T-Lymphocyte Subsets/classification; Up-Regulation  
  Abstract Using gene expression profiling, we show here that activation of B cells and professional antigen-presenting cells (APCs) induces the expression of common chemokines. Among these, CCL4 was the most potent chemoattractant of a CD4+CD25+ T cell population, which is a characteristic phenotype of regulatory T cells. Depletion of either regulatory T cells or CCL4 resulted in a deregulated humoral response, which culminated in the production of autoantibodies. This suggested that the recruitment of regulatory T cells to B cells and APCs by CCL4 plays a central role in the normal initiation of T cell and humoral responses, and failure to do this leads to autoimmune activation.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Medical Research Council, Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK. Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes 1529-2908Journal Article Approved no  
  Call Number MRC @ kga @ Bystry2001 Serial 95  
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Author Salomon, B.; Lenschow, D.J.; Rhee, L.; Ashourian, N.; Singh, B.; Sharpe, A.; Bluestone, J.A. url  openurl
  Title B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes Type Journal Article
  Year 2000 Publication Immunity Abbreviated Journal  
  Volume 12 Issue 4 Pages 431-440  
  Keywords  
  Abstract CD28/B7 costimulation has been implicated in the induction and progression of autoimmune diseases. Experimentally induced models of autoimmunity have been shown to be prevented or reduced in intensity in mice rendered deficient for CD28 costimulation. In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. These mice present a profound decrease of the immunoregulatory CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice. These cells are absent from both CD28KO and B7-1/B7-2KO mice, and the transfer of this regulatory T cell subset from control NOD animals into CD28-deficient animals can delay/prevent diabetes. The results suggest that the CD28/ B7 costimulatory pathway is essential for the development and homeostasis of regulatory T cells that control spontaneous autoimmune diseases.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Committee on Immunology, Ben May Institute for Cancer Research and Department of Pathology, Universi Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Salomon2000 Serial 96  
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Author Kullberg, M.C.; Jankovic, D.; Gorelick, P.L.; Caspar, P.; Letterio, J.J.; Cheever, A.W.; Sher, A. url  openurl
  Title Bacteria-triggered CD4(+) T regulatory cells suppress Helicobacter hepaticus-induced colitis Type Journal Article
  Year 2002 Publication J Exp Med Abbreviated Journal  
  Volume 196 Issue 4 Pages 505-515  
  Keywords Adoptive Transfer; Animals; Antigens, Bacterial/immunology; Antigens, CD45/immunology; Biological Markers; CD4-Positive T-Lymphocytes/cytology/*immunology; Colitis/*immunology; DNA-Binding Proteins/genetics/immunology; Female; Helicobacter/immunology; Helicobacter Infections/*immunology; Interleukin-10/genetics/immunology; Interleukin-4/genetics/immunology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Receptors, Interleukin-2; Research Support, U.S. Gov't, P.H.S.; Transforming Growth Factor beta/immunology  
  Abstract We have previously demonstrated that interleukin (IL)-10-deficient (IL-10 knockout [KO]) but not wild-type (WT) mice develop colitis after infection with Helicobacter hepaticus. Here, we show that infected recombination activating gene (RAG) KO mice develop intestinal inflammation after reconstitution with CD4(+) T cells from IL-10 KO animals and that the cotransfer of CD4(+) T cells from H. hepaticus-infected but not uninfected WT mice prevents this colitis. The disease-protective WT CD4(+) cells are contained within the CD45RB(low) fraction and unexpectedly were found in both the CD25(+) and the CD25(-) subpopulations of these cells, their frequency being higher in the latter. The mechanism by which CD25(+) and CD25(-) CD45RB(low) CD4(+) cells block colitis involves IL-10 and not transforming growth factor (TGF)-beta, as treatment with anti-IL-10R but not anti-TGF-beta monoclonal antibody abrogated their protective effect. In vitro, CD45RB(low) CD4(+) cells from infected WT mice were shown to produce IL-10 and suppress interferon-gamma production by IL-10 KO CD4(+) cells in an H. hepaticus antigen-specific manner. Together, our data support the concept that H. hepaticus infection results in the induction in WT mice of regulatory T cells that prevent bacteria-induced colitis. The induction of such cells in response to gut flora may be a mechanism protecting normal individuals against inflammatory bowel disease.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectiou Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes 0022-1007Journal Article Approved no  
  Call Number MRC @ kga @ Kullberg2002 Serial 97  
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Author Chen, X.; Oppenheim, J.J.; Howard, O.M. url  openurl
  Title BALB/c mice have more CD4+CD25+ T regulatory cells and show greater susceptibility to suppression of their CD4+CD25- responder T cells than C57BL/6 mice Type Journal Article
  Year 2005 Publication J Leukoc Biol Abbreviated Journal  
  Volume 78 Issue 1 Pages 114-121  
  Keywords  
  Abstract Increasing evidence indicates that CD4(+)CD25(+) T regulatory (Treg) cells control a wide spectrum of immune responses. The initial identification of CD4(+)CD25(+) Treg cell as a “professional suppressor” was based on observations made in BALB/c mice. This mouse strain is well known to preferentially develop T helper cell type 2 responses, to be more susceptible to intracellular parasite infection, to have a higher tumor incidence, and to be more resistant to the induction of autoimmune diseases, as compared with C57BL/6 (B6) mice. We therefore decided to compare Treg cell function of B6 and BALB/c mice. We observed that the frequency of CD4(+)CD25(+) T cells in the thymus and peripheral lymphoid organs of BALB/c mice was higher than in B6 mice. CD4(+)CD25(+) Treg cells from both mouse strains shared similar phenotypic properties, including expression of characteristic immunological markers and hyporesponsiveness to T cell receptor cross-linking and in their capacity to suppress proliferation of BALB/c CD4(+)CD25(-) T responder (Tres) cells. However, CD4(+)CD25(-) Tres cells from B6 mice were notably less susceptible to suppression by CD4(+)CD25(+) Treg cells from either mouse strain. Our data suggest that the number and the level of suppression of CD4(+)CD25(+) Treg cells for CD4(+)CD25(-) Tres cells may be dictated by genetic background. Our data also suggest that differences in the CD4(+)CD25(+) Treg cell number and the susceptibility of CD4(+)CD25(-) Tres cells may, at least in part, account for the differences in immune response between B6 and BALB/c strains of mice.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Basic Research Program, SAIC-Frederick, Inc., MD 21702, USA. xinc@ncifcrf.gov Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes 0741-5400Journal Article Approved no  
  Call Number MRC @ kga @ Chen2005 Serial 98  
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Author Vernochet, C.; Caucheteux, S.M.; Kanellopoulos-Langevin, C. url  openurl
  Title Bi-directional Cell Trafficking Between Mother and Fetus in Mouse Placenta Type Journal Article
  Year 2006 Publication Placenta Abbreviated Journal  
  Volume Issue Pages  
  Keywords  
  Abstract It is now well established that cells are exchanged between mother and fetus during gestation. It has been proposed that some of these exchanges take place in the placenta, but it has never been demonstrated. Here, we made use of EGFP (Enhanced Green Fluorescent Protein) transgenic mice to precisely visualize the juxtaposition of maternal and fetal tissues at the implantation site, as well as to describe the bi-directional cell trafficking between mother and fetus at different stages of gestation. The influence of genetic differences between mother and fetus on the cell migration was also addressed by studying various types of matings: syngeneic, allogeneic and outbred. The frequency of maternal-fetal cell exchanges within the placenta is much higher in syngeneic and allogeneic gestations than in outbred ones. Maternal cells were mainly localized in the labyrinth where they were scattered or sometimes grouped in or near blood spaces. Groups of maternal cells could also be observed in maternal blood sinuses of the spongiotrophoblast. Conversely, fetal cells were organized in rings surrounding maternal blood sinuses in the decidua at 10-12days of gestation. After day 13, they invaded the decidua. Fetal cells could also be detected in maternal peripheral blood and organs by nested PCR and fluorescence microscopy on cryosections, respectively. This suggests a role in the establishment and maintenance of the maternal tolerance to the fetus.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Laboratory of Immune Regulations and Development, Department of Developmental Biology, J. Monod Inst Editor  
  Language (up) Summary Language Original Title  
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  ISSN ISBN Medium  
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  Notes Approved no  
  Call Number MRC @ kga @ Vernochet2006 Serial 99  
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Author Hardy, J.; Edinger, M.; Bachmann, M.H.; Negrin, R.S.; Fathman, C.G.; Contag, C.H. url  openurl
  Title Bioluminescence imaging of lymphocyte trafficking in vivo Type Journal Article
  Year 2001 Publication Exp Hematol Abbreviated Journal  
  Volume 29 Issue 12 Pages 1353-1360  
  Keywords  
  Abstract Lymphocytes are highly mobile cells that travel throughout the body in response to a tremendous variety of stimuli. Revealing lymphocyte trafficking patterns in vivo is necessary for a complete understanding of immune function, as well as cell-cell and cell-tissue interactions in immune development and in response to insult. Although the location of cell populations in various tissues at any given point in time may be revealed by techniques such as flow cytometry and immunofluorescence, these methods are not readily amenable to the assessment of dynamic cell migration patterns in vivo. In the past 5 years, technologies for imaging molecular and cellular changes in living animals have advanced to a point where it is possible to reveal the migratory paths of these vitally important cells. Here, we review one advancement in cellular imaging, in vivo bioluminescence imaging, which addresses the problem of lymphocyte tracking. This imaging strategy has the potential to elucidate the temporal patterns of immune responses and the spatial distribution of lymphocytes within the body.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Department of Pediatrics, Stanford University School of Medicine, Stanford, Calif., USA. Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Hardy2001 Serial 100  
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Author Shapiro-Shelef, M.; Lin, K.I.; McHeyzer-Williams, L.J.; Liao, J.; McHeyzer-Williams, M.G.; Calame, K. url  openurl
  Title Blimp-1 is required for the formation of immunoglobulin secreting plasma cells and pre-plasma memory B cells Type Journal Article
  Year 2003 Publication Immunity Abbreviated Journal  
  Volume 19 Issue 4 Pages 607-620  
  Keywords  
  Abstract Blimp-1 is a transcriptional repressor able to drive the terminal differentiation of B cells into Ig-secreting plasma cells. We have created mice with a B cell-specific deletion of prdm1, the gene encoding Blimp-1. B cell development and the number of B cells responding to antigen appear to be normal in these mice. However, in response to either TD or TI antigen, serum Ig, short-lived plasma cells, post-GC plasma cells, and plasma cells in a memory response are virtually absent, demonstrating that Blimp-1 is required for plasmacytic differentiation and Ig secretion. In the absence of Blimp-1, CD79b(+)B220(-) pre-plasma memory B cell development is also defective, providing evidence that this subset is an intermediate in plasma cell development. B cells lacking Blimp-1 cannot secrete Ig or induce muS mRNA when stimulated ex vivo. Furthermore, although prdm1-/- B cells fail to induce XBP-1, XBP-1 cannot rescue plasmacytic differentiation without Blimp-1.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 100 Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
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  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Shapiro-Shelef2003 Serial 101  
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Author Turner, C.A.J.; Mack, D.H.; Davis, M.M. url  openurl
  Title Blimp-1, a novel zinc finger-containing protein that can drive the maturation of B lymphocytes into immunoglobulin-secreting cells Type Journal Article
  Year 1994 Publication Cell Abbreviated Journal  
  Volume 77 Issue 2 Pages 297-306  
  Keywords  
  Abstract We describe a novel gene, Blimp-1 (for B lymphocyte-induced maturation protein), transcripts of which are rapidly induced during the differentiation of B lymphocytes into immunoglobulin secretory cells and whose expression is characteristic of late B and plasma cell lines. The 856 amino acid open reading frame contains five Kruppel-type zinc finger motifs and proline-rich and acidic regions similar to those of known transcription factors. Serological studies show an approximately 100 kd protein that localizes to the nucleus. Stable or transient transfection of Blimp-1 into B cell lymphoma lines leads to the expression of many of the phenotypic changes associated with B cell differentiation into an early plasma cell stage, including induction of J chain message and immunoglobulin secretion, up-regulation of Syndecan-1, and increased cell size and granularity. Thus, Blimp-1 appears to be a pleiotropic regulatory factor capable of at least partially driving the terminal differentiation of B cells.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Howard Hughes Medical Institute, Stanford University School of Medicine, California 94305-5428. Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
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  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Turner1994 Serial 102  
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Author Jin, L.P.; Zhou, Y.H.; Wang, M.Y.; Zhu, X.Y.; Li, D.J. url  openurl
  Title Blockade of CD80 and CD86 at the time of implantation inhibits maternal rejection to the allogeneic fetus in abortion-prone matings Type Journal Article
  Year 2005 Publication J Reprod Immunol Abbreviated Journal  
  Volume 65 Issue 2 Pages 133-146  
  Keywords  
  Abstract CD28/CTLA-4 interactions with their specific B7-ligands (CD80 and CD86) play a decisive role in antigenic and allogenic responses. Recently, experimental transplant studies demonstrated that donor-specific tolerance was achieved by blocking these interactions. However, the role of blockade of CD28/B7 costimulatory pathway in the maintenance of materno-fetal tolerance has received little attention. In the present study, abortion-prone CBA/J females mated with DBA/2 males were administered with anti-CD80 and anti-CD86 monoclonal antibodies (mAbs) on day 4 of gestation (time of murine implantation). We demonstrated that the combined use of anti-CD80 and anti-CD86 mAbs induced maternal tolerance to the fetus in the abortion-prone CBA/J mice, and displayed expansion of the maternal CD4(+)CD25+ regulatory T cell population and up-regulated expression of CTLA-4, suggesting an active mechanism of regulatory T cells in suppressing maternal rejection to the fetus. In addition, the anti-CD80/86 mAbs treatment enhanced Th2 and reduced Th1 cytokine production in mice, implying that the development of Th2 cells might contribute to maternal tolerance to her fetus. Together, these findings indicated that blocking CD80 and CD86 enhanced maternal tolerance to her fetus in mice by increasing regulatory T cell function and skewing toward a Th2 response. Our data might provide an enhanced understanding of the maternal-fetal immune relationship and be helpful in clinical trials for immunotherapy of recurrent spontaneous abortion.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Laboratory for Reproductive Immunology, Institute of Obstetrics and Gynecology, Fudan University, 41 Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Jin2005 Serial 103  
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Author Read, S.; Greenwald, R.; Izcue, A.; Robinson, N.; Mandelbrot, D.; Francisco, L.; Sharpe, A.H.; Powrie, F. url  openurl
  Title Blockade of CTLA-4 on CD4+CD25+ regulatory T cells abrogates their function in vivo Type Journal Article
  Year 2006 Publication J Immunol Abbreviated Journal  
  Volume 177 Issue 7 Pages 4376-4383  
  Keywords  
  Abstract Naturally occurring CD4+ regulatory T cells (T(R)) that express CD25 and the transcription factor FoxP3 play a key role in immune homeostasis, preventing immune pathological responses to self and foreign Ags. CTLA-4 is expressed by a high percentage of these cells, and is often considered as a marker for T(R) in experimental and clinical analysis. However, it has not yet been proven that CTLA-4 has a direct role in T(R) function. In this study, using a T cell-mediated colitis model, we demonstrate that anti-CTLA-4 mAb treatment inhibits T(R) function in vivo via direct effects on CTLA-4-expressing T(R), and not via hyperactivation of colitogenic effector T cells. Although anti-CTLA-4 mAb treatment completely inhibits T(R) function, it does not reduce T(R) numbers or their homing to the GALT, suggesting the Ab mediates its function by blockade of a signal required for T(R) activity. In contrast to the striking effect of the Ab, CTLA-4-deficient mice can produce functional T(R), suggesting that under some circumstances other immune regulatory mechanisms, including the production of IL-10, are able to compensate for the loss of the CTLA-4-mediated pathway. This study provides direct evidence that CTLA-4 has a specific, nonredundant role in the function of normal T(R). This role has to be taken into account when targeting CTLA-4 for therapeutic purposes, as such a strategy will not only boost effector T cell responses, but might also break T(R)-mediated self-tolerance.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, United Kingdom Editor  
  Language (up) Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number MRC @ kga @ Read2006 Serial 104  
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