2024-03-28T17:56:28Zhttp://repository.helmholtz-hzi.de/oai/requestoai:repository.helmholtz-hzi.de:10033/85982019-08-30T11:32:38Zcom_10033_6800com_10033_6799col_10033_6875
In Vivo Effects of a Synthetic 2-Kilodalton Macrophage-Activating Lipopeptide of Mycoplasma fermentans after Pulmonary Application
Lührmann, Anke
Deiters, Ursula
Skokowa, Julia
Hanke, Michaela
Gessner, Johannes E.
Mühlradt, Peter F.
Pabst, Reinhard
Tschernig, Thomas
2007-02-20T12:50:48Z
2002-07
2007-02-20T12:50:48Z
2002-07
Infection and Immunity 2002 70(7):3785-3792
0019-9567
1098-5522
12065522
10.1128/IAI.70.7.3785-3792.2002
http://hdl.handle.net/10033/8598
128036
en_US
Copyright © 2002, American Society for Microbiology
American Society for Microbiology
oai:repository.helmholtz-hzi.de:10033/86132019-08-30T11:25:04Zcom_10033_6800com_10033_6799col_10033_6875
Involvement of interleukin-1 (IL-1), IL-6, IL-2, and IL-4 in generation of cytolytic T cells from thymocytes stimulated by a Mycoplasma fermentans-derived product.
Mühlradt, P F
Quentmeier, H
Schmitt, E
2007-02-20T13:09:16Z
1991-11
2007-02-20T13:09:16Z
1991-11
Infection and Immunity 1991 59(11):3962-3968
0019-9567
1098-5522
1937754
http://hdl.handle.net/10033/8613
258983
en_US
oai:repository.helmholtz-hzi.de:10033/86152019-08-30T11:25:04Zcom_10033_6800com_10033_6799col_10033_6875
MDHM, a macrophage-stimulatory product of Mycoplasma fermentans, leads to in vitro interleukin-1 (IL-1), IL-6, tumor necrosis factor, and prostaglandin production and is pyrogenic in rabbits.
Mühlradt, P F
Schade, U
2007-02-20T13:10:30Z
1991-11
2007-02-20T13:10:30Z
1991-11
Infection and Immunity 1991 59(11):3969-3974
0019-9567
1098-5522
1937755
http://hdl.handle.net/10033/8615
258984
en_US
oai:repository.helmholtz-hzi.de:10033/86272019-08-30T11:26:12Zcom_10033_6800com_10033_6799col_10033_6875
Purification and partial biochemical characterization of a Mycoplasma fermentans-derived substance that activates macrophages to release nitric oxide, tumor necrosis factor, and interleukin-6.
Mühlradt, P F
Frisch, M
Images
2007-02-20T13:25:21Z
1994-09
2007-02-20T13:25:21Z
1994-09
Infection and Immunity 1994 62(9):3801-3807
0019-9567
1098-5522
8063396
http://hdl.handle.net/10033/8627
303034
en_US
oai:repository.helmholtz-hzi.de:10033/86422019-08-30T11:25:04Zcom_10033_6800com_10033_6799col_10033_6875
Mycoplasma fermentans-derived high-molecular-weight material induces interleukin-6 release in cultures of murine macrophages and human monocytes.
Quentmeier, H
Schmitt, E
Kirchhoff, H
Grote, W
Mühlradt, P F
2007-02-20T13:36:12Z
1990-05
2007-02-20T13:36:12Z
1990-05
Infection and Immunity 1990 58(5):1273-1280
0019-9567
1098-5522
2323816
http://hdl.handle.net/10033/8642
258620
en_US
oai:repository.helmholtz-hzi.de:10033/86432019-08-30T11:24:25Zcom_10033_6800com_10033_6799col_10033_6875
Effects of pyocyanine, a phenazine dye from Pseudomonas aeruginosa, on oxidative burst and bacterial killing in human neutrophils.
Müller, P K
Krohn, K
Mühlradt, P F
2007-02-20T13:36:37Z
1989-09
2007-02-20T13:36:37Z
1989-09
Infection and Immunity 1989 57(9):2591-2596
0019-9567
1098-5522
2547716
http://hdl.handle.net/10033/8643
313499
en_US
oai:repository.helmholtz-hzi.de:10033/86462019-08-30T11:25:38Zcom_10033_6800com_10033_6799col_10033_6875
The p53-dependent effects of macrophage migration inhibitory factor revealed by gene targeting
Fingerle-Rowson, G.
Petrenko, O.
Metz, C. N.
Forsthuber, T. G.
Mitchell, R.
Huss, R.
Moll, U.
Müller, W.
Bucala, R.
2007-02-20T13:37:53Z
2003-08-05
2007-02-20T13:37:53Z
2003-08-05
Proceedings of the National Academy of Sciences of the United States of America 2003 100(16):9354-9359
0027-8424
1091-6490
12878730
10.1073/pnas.1533295100
http://hdl.handle.net/10033/8646
170922
en_US
Copyright © 2003, The National Academy of
Sciences
National Academy of Sciences
oai:repository.helmholtz-hzi.de:10033/86802019-08-30T11:32:36Zcom_10033_6800com_10033_6799col_10033_6875
Pre-B cell receptor expression is necessary for thymic stromal lymphopoietin responsiveness in the bone marrow but not in the liver environment
Vosshenrich, Christian A. J.
Cumano, Ana
Müller, Werner
Di Santo, James P.
Vieira, Paulo
2007-02-21T08:16:20Z
2004-07-27
2007-02-21T08:16:20Z
2004-07-27
Proceedings of the National Academy of Sciences of the United States of America 2004 101(30):11070-11075
0027-8424
1091-6490
15263090
10.1073/pnas.0402919101
http://hdl.handle.net/10033/8680
503742
en_US
Copyright © 2004, The National Academy of Sciences
National Academy of Sciences
oai:repository.helmholtz-hzi.de:10033/145182019-08-30T11:34:48Zcom_10033_6800com_10033_6799col_10033_6875
Adult murine hematopoiesis can proceed without beta1 and beta7 integrins.
Bungartz, Gerd
Stiller, Sebastian
Bauer, Martina
Müller, Werner
Schippers, Angela
Wagner, Norbert
Fässler, Reinhard
Brakebusch, Cord
The function of alpha4beta1 and alpha4beta7 integrins in hematopoiesis is controversial. While some experimental evidence suggests a crucial role for these integrins in retention and expansion of progenitor cells and lymphopoiesis, others report a less important role in hematopoiesis. Using mice with a deletion of the beta1 and the beta7 integrin genes restricted to the hematopoietic system we show here that alpha4beta1 and alpha4beta7 integrins are not essential for differentiation of lymphocytes or myelocytes. However, beta1beta7 mutant mice displayed a transient increase of colony-forming unit (CFU-C) progenitors in the bone marrow and, after phenylhydrazine-induced anemia, a decreased number of splenic erythroid colony-forming units in culture (CFUe's). Array gene expression analysis of CD4(+)CD8(+) double-positive (DP) and CD4(-)CD8(-) double-negative (DN) thymocytes and CD19(+) and CD4(+) splenocytes did not provide any evidence for a compensatory mechanism explaining the mild phenotype. These data show that alpha4beta1 and alpha4beta7 are not required for blood cell differentiation, although in their absence alterations in numbers and distribution of progenitor cells were observed.
2007-11-13T09:30:25Z
2007-11-13T09:30:25Z
2006-09-15
Article
Blood 2006, 108(6):1857-64
0006-4971
16735603
10.1182/blood-2005-10-007658
http://hdl.handle.net/10033/14518
en
oai:repository.helmholtz-hzi.de:10033/146272019-08-30T11:35:13Zcom_10033_6800com_10033_6799col_10033_6875
Interleukin-10 derived from macrophages and/or neutrophils regulates the inflammatory response to LPS but not the response to CpG DNA.
Siewe, Lisa
Bollati-Fogolin, Mariela
Wickenhauser, Claudia
Krieg, Thomas
Müller, Werner
Roers, Axel
Interleukin-10 (IL-10) is an important regulator of immune responses secreted by different cell types. We have previously shown that mice with selective inactivation of the IL-10 gene in T cells suffer from deregulated T cell responses similar to those observed in IL-10(-/-) animals. Unlike IL-10(-/-) mice, however, T cell-specific mutants do not mount an enhanced innate immune response to LPS, which must, therefore, be subject to control by IL-10 from non-T cells. Herein we show that subcutaneous injection of LPS, which causes moderate local inflammation in WT and T cell-specific IL-10 mutant mice, results in augmented inflammatory infiltration and extensive tissue necrosis in mice with deficiency for IL-10 in macrophages and neutrophils. Correspondingly, we observed an enhanced sensitivity of the macrophage/neutrophil-specific IL-10 mutants to systemic LPS exposure when compared with WT animals. In contrast, the inflammatory response of these mutants to CpG oligodeoxynucleotides was not different from that of WT mice. While IL-10(-/-) mice developed massive inflammation, necrosis and increased serum cytokine levels after subcutaneous CpG injection, only moderate responses were observed in macrophage/neutrophil-specific IL-10 mutant and WT mice. These results show that different innate immune responses can be subject to control by IL-10 from different cellular sources.
2007-11-19T13:25:55Z
2007-11-19T13:25:55Z
2006-12-01
Article
Eur. J. Immunol. 2006, 36(12):3248-55
0014-2980
17111348
10.1002/eji.200636012
http://hdl.handle.net/10033/14627
en
oai:repository.helmholtz-hzi.de:10033/221732019-08-30T11:34:48Zcom_10033_6800com_10033_6799col_10033_6875
Serum response factor contributes selectively to lymphocyte development.
Fleige, Anne
Alberti, Siegfried
Gröbe, Lothar
Frischmann, Ursula
Geffers, Robert
Müller, Werner
Nordheim, Alfred
Schippers, Angela
Department of Experimental Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Serum response factor (SRF), is a crucial transcription factor for murine embryonic development and for the function of muscle cells and neurons. Gene expression data show that SRF and its transcriptional cofactors are also expressed in lymphocyte precursors and mature lymphocytes. However, the role of SRF in lymphocyte development has not been addressed in vivo so far, attributed in part to early embryonic lethality of conventional Srf-null mice. To determine the in vivo role of SRF in developing lymphocytes, we specifically inactivated the murine Srf gene during T or B cell development using lymphocyte-specific Cre transgenic mouse lines. T cell-specific Srf deletion led to a severe block in thymocyte development at the transition from CD4/CD8 double to single positive stage. The few residual T cells detectable in the periphery retained at least one functional Srf allele, thereby demonstrating the importance of SRF in T cell development. In contrast, deletion of Srf in developing B cells did not interfere with the growth and survival of B cells in general, yet led to a complete loss of marginal zone B cells and a marked reduction of the CD5+ B cell subset. Our study also revealed a contribution of SRF to the expression of the surface molecules IgM, CD19, and the chemokine receptor 4 in B lymphocytes. We conclude that SRF fulfills essential and distinct functions in the differentiation of different types of lymphocytes.
2008-04-03T08:37:01Z
2008-04-03T08:37:01Z
2007-08-17
Article
Serum response factor contributes selectively to lymphocyte development. 2007, 282 (33):24320-8 J. Biol. Chem.
0021-9258
17591768
10.1074/jbc.M703119200
http://hdl.handle.net/10033/22173
The Journal of biological chemistry
en
oai:repository.helmholtz-hzi.de:10033/223532019-08-30T11:37:23Zcom_10033_6800com_10033_6799col_10033_6875
MUGEN mouse database; animal models of human immunological diseases.
Aidinis, V
Chandras, C
Manoloukos, M
Thanassopoulou, A
Kranidioti, K
Armaka, M
Douni, E
Kontoyiannis, D L
Zouberakis, M
Kollias, G
B.S.R.C. Alexander Fleming, 34 Fleming Street, 16672, Vari, Greece. v.aidinis@fleming.gr
The MUGEN mouse database (MMdb) (www.mugen-noe.org/database/) is a database of murine models of immune processes and immunological diseases. Its aim is to share and publicize information on mouse strain characteristics and availability from participating institutions. MMdb's basic classification of models is based on three major research application categories: Models of Human Disease, Models of Immune Processes and Transgenic Tools. Data on mutant strains includes detailed information on affected gene(s), mutant allele(s) and genetic background (DNA origin, gene targeted, host and backcross strain background). Each gene/transgene index also includes IDs and direct links to Ensembl, ArrayExpress, EURExpress and NCBI's Entrez Gene database. Phenotypic description is standardized and hierarchically structured, based on MGI's mammalian phenotypic ontology terms. Availability (e.g. live mice, cryopreserved embryos, sperm and ES cells) is clearly indicated, along with handling and genotyping details (in the form of documents or hyperlinks) and all relevant contact information (including EMMA and Jax/IMSR hyperlinks where available). MMdb's design offers a user-friendly query interface and provides instant access to the list of mutant strains and genes. Database access is free of charge and there are no registration requirements for data querying.
2008-04-04T14:39:02Z
2008-04-04T14:39:02Z
2008-01
Article
MUGEN mouse database; animal models of human immunological diseases. 2008, 36 (Database issue):D1048-54 Nucleic Acids Res.
1362-4962
17932065
10.1093/nar/gkm838
http://hdl.handle.net/10033/22353
Nucleic acids research
en
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17932065
oai:repository.helmholtz-hzi.de:10033/234322019-08-30T11:37:23Zcom_10033_6800com_10033_6799col_10033_6875
LMP1 signaling can replace CD40 signaling in B cells in vivo and has unique features of inducing class-switch recombination to IgG1.
Rastelli, Julia
Hömig-Hölzel, Cornelia
Seagal, Jane
Müller, Werner
Hermann, Andrea C
Rajewsky, Klaus
Zimber-Strobl, Ursula
Institute of Clinical Molecular Biology and Tumor Genetics, GSF-National Research Center for Environment and Health, Munich, Germany.
The Epstein-Barr virus (EBV) protein LMP1 is considered to be a functional homologue of the CD40 receptor. However, in contrast to the latter, LMP1 is a constitutively active signaling molecule. To compare B cell-specific LMP1 and CD40 signaling in an unambiguous manner, we generated transgenic mice conditionally expressing a CD40/LMP1 fusion protein, which retained the LMP1 cytoplasmic tail but has lost the constitutive activity of LMP1 and needs to be activated by the CD40 ligand. We show that LMP1 signaling can completely substitute CD40 signaling in B cells, leading to normal B-cell development, activation, and immune responses including class-switch recombination, germinal center formation, and somatic hypermutation. In addition, the LMP1-signaling domain has a unique property in that it can induce class-switch recombination to IgG1 independent of cytokines. Thus, our data indicate that LMP1 has evolved to imitate T-helper cell function allowing activation, proliferation, and differentiation of EBV-infected B cells independent of T cells.
2008-04-15T12:32:49Z
2008-04-15T12:32:49Z
2008-02-01
Article
LMP1 signaling can replace CD40 signaling in B cells in vivo and has unique features of inducing class-switch recombination to IgG1. 2008, 111 (3):1448-55 Blood
0006-4971
18006702
10.1182/blood-2007-10-117655
http://hdl.handle.net/10033/23432
Blood
en
oai:repository.helmholtz-hzi.de:10033/362122019-08-30T11:31:49Zcom_10033_6800com_10033_6799col_10033_6875
Constitutive CD40 signaling in B cells selectively activates the noncanonical NF-kappaB pathway and promotes lymphomagenesis.
Hömig-Hölzel, Cornelia
Hojer, Caroline
Rastelli, Julia
Casola, Stefano
Strobl, Lothar J
Müller, Werner
Quintanilla-Martinez, Leticia
Gewies, Andreas
Ruland, Jürgen
Rajewsky, Klaus
Zimber-Strobl, Ursula
Institute of Clinical Molecular Biology and Tumor Genetics, Helmholtz Center Munich, German Research Center for Environment and Health, D-81377 Munich, Germany.
CD40, a member of the tumor necrosis factor (TNF) receptor family, plays an essential role in T cell-dependent immune responses. Because CD40 is widely expressed on the surface of tumor cells in various B cell malignancies, deregulated CD40 signaling has been suggested to contribute to lymphomagenesis. In this study, we show that B cell-specific expression of a constitutively active CD40 receptor, in the form of a latent membrane protein 1 (LMP1)/CD40 chimeric protein, promoted an increase in the number of follicular and marginal zone B cells in secondary lymphoid organs in transgenic mice. The B cells displayed an activated phenotype, prolonged survival and increased proliferation, but were significantly impaired in T cell-dependent immune responses. Constitutive CD40 signaling in B cells induced selective and constitutive activation of the noncanonical NF-kappaB pathway and the mitogen-activated protein kinases Jnk and extracellular signal-regulated kinase. LMP1/CD40-expressing mice older than 12 mo developed B cell lymphomas of mono- or oligoclonal origin at high incidence, thus showing that the interplay of the signaling pathways induced by constitutive CD40 signaling is sufficient to initiate a tumorigenic process, ultimately leading to the development of B cell lymphomas.
2008-08-22T08:58:57Z
2008-08-22T08:58:57Z
2008-06-09
Article
Constitutive CD40 signaling in B cells selectively activates the noncanonical NF-kappaB pathway and promotes lymphomagenesis. 2008, 205 (6):1317-29 J. Exp. Med.
1540-9538
18490492
10.1084/jem.20080238
http://hdl.handle.net/10033/36212
The Journal of experimental medicine
en
oai:repository.helmholtz-hzi.de:10033/483942019-08-30T11:32:16Zcom_10033_6800com_10033_6799col_10033_6875
Mouse Phenotype Database Integration Consortium: integration [corrected] of mouse phenome data resources.
Hancock, John M
Adams, Niels C
Aidinis, Vassilis
Blake, Andrew
Bogue, Molly
Brown, Steve D M
Chesler, Elissa J
Davidson, Duncan
Duran, Christopher
Eppig, Janan T
Gailus-Durner, Valérie
Gates, Hilary
Gkoutos, Georgios V
Greenaway, Simon
Hrabé de Angelis, Martin
Kollias, George
Leblanc, Sophie
Lee, Kirsty
Lengger, Christoph
Maier, Holger
Mallon, Ann-Marie
Masuya, Hiroshi
Melvin, David G
Müller, Werner
Parkinson, Helen
Proctor, Glenn
Reuveni, Eli
Schofield, Paul
Shukla, Aadya
Smith, Cynthia
Toyoda, Tetsuro
Vasseur, Laurent
Wakana, Shigeharu
Walling, Alison
White, Jacqui
Wood, Joe
Zouberakis, Michalis
Understanding the functions encoded in the mouse genome will be central to an understanding of the genetic basis of human disease. To achieve this it will be essential to be able to characterize the phenotypic consequences of variation and alterations in individual genes. Data on the phenotypes of mouse strains are currently held in a number of different forms (detailed descriptions of mouse lines, first-line phenotyping data on novel mutations, data on the normal features of inbred lines) at many sites worldwide. For the most efficient use of these data sets, we have initiated a process to develop standards for the description of phenotypes (using ontologies) and file formats for the description of phenotyping protocols and phenotype data sets. This process is ongoing and needs to be supported by the wider mouse genetics and phenotyping communities to succeed. We invite interested parties to contact us as we develop this process further.
2009-02-03T15:13:12Z
2009-02-03T15:13:12Z
2007-03
Article
Mouse Phenotype Database Integration Consortium: integration [corrected] of mouse phenome data resources. 2007, 18 (3):157-63 Mamm. Genome
0938-8990
17436037
10.1007/s00335-007-9004-x
http://hdl.handle.net/10033/48394
Mammalian genome : official journal of the International Mammalian Genome Society
en
oai:repository.helmholtz-hzi.de:10033/711182019-08-30T11:34:22Zcom_10033_6800com_10033_6799col_10033_6875
Maternal farm exposure modulates neonatal immune mechanisms through regulatory T cells.
Schaub, Bianca
Liu, Jing
Höppler, Sabine
Schleich, Isolde
Huehn, Jochen
Olek, Sven
Wieczorek, Georg
Illi, Sabina
von Mutius, Erika
Department of Pulmonary and Allergy, University Children's Hospital Munich, LMU Munich, Munich, Germany. Bianca.Schaub@med.uni-muenchen.de
BACKGROUND: Cross-sectional studies suggest that maternal exposure to farming decreases the risk of allergic diseases in offspring. The potential underlying immunologic mechanisms are not understood. OBJECTIVE: We sought to assess whether maternal farm exposure activates regulatory T (Treg) cells in cord blood, exerting T(H)2-suppressive effects after microbial stimulation. METHODS: Eighty-four pregnant mothers were recruited before delivery. Detailed questionnaires (60 nonfarming and 22 farming mothers with 2 exclusions) assessed the farming exposures. Cord blood was stimulated with the microbial stimulus peptidoglycan (Ppg), the mitogen PHA, house dust mite extracts (Der p 1), and combinations. Treg cells (CD4+CD25(high) cells; intracellular forkhead/winged-helix family transcriptional repressor p3 [FOXP3] expression, FOXP3 levels, lymphocyte activation gene 3 mRNA expression, functional studies, and DNA methylation of the FOXP3 locus), proliferation, and T(H)2/T(H)1/T(H)17 cytokines were examined. RESULTS: Cord blood Treg cell counts (both unstimulated and PHA stimulated) were increased with maternal farming exposures and associated with higher FOXP3 (Der p 1 + Ppg stimulation) and trendwise higher lymphocyte activation gene 3 (Ppg) expression. Furthermore, Treg cell function was more efficient with farming exposure (effector cell suppression, P = .004). In parallel, T(H)2 cytokine (IL-5) levels were decreased and associated with decreased lymphoproliferation and increased IL-6 levels (Ppg stimulation, Der p 1 + Ppg stimulation, or both; P < .05). Maternal exposure to increasing numbers of farm animals and stables was discovered to exert distinct effects on Treg cells, T(H)1/T(H)2 cells, or both. Additionally, FOXP3 demethylation in offspring of mothers with farm milk exposure was increased (P = .02). CONCLUSIONS: Farm exposures during pregnancy increase the number and function of cord blood Treg cells associated with lower T(H)2 cytokine secretion and lymphocyte proliferation on innate exposure. One fascinating speculation is that maternal farm exposure might reflect a natural model of immunotherapy, potentially including a selection of innate stimuli in addition to allergen, shaping a child's immune system at an early stage.
2009-06-22T13:20:17Z
2009-06-22T13:20:17Z
2009-04
Article
Maternal farm exposure modulates neonatal immune mechanisms through regulatory T cells. 2009, 123 (4):774-82.e5 J. Allergy Clin. Immunol.
1097-6825
19348917
10.1016/j.jaci.2009.01.056
http://hdl.handle.net/10033/71118
The Journal of allergy and clinical immunology
en