U Steinhoff

Summary

Affiliation: Max-Planck-Institute for Infection Biology
Country: Germany

Publications

  1. ncbi Altered intestinal immune system but normal antibacterial resistance in the absence of P-selectin and ICAM-1
    U Steinhoff
    Department of Immunology, Max Planck Institute of Infection Biology, Berlin, Germany
    J Immunol 160:6112-20. 1998
  2. ncbi Who controls the crowd? New findings and old questions about the intestinal microflora
    Ulrich Steinhoff
    Max Planck Institute of Infection Biology, 10117 Berlin, Germany
    Immunol Lett 99:12-6. 2005
  3. ncbi Leprosy susceptibility-a matter of protein degradation? The role of proteasomes in infection and disease
    Ulrich Steinhoff
    Max Planck Institute of Infection Biology, Berlin, Germany
    Int J Lepr Other Mycobact Dis 73:135-7. 2005
  4. ncbi Autoimmune intestinal pathology induced by hsp60-specific CD8 T cells
    U Steinhoff
    Department of Immunology, Max Planck Institute of Infection Biology, Germany
    Immunity 11:349-58. 1999
  5. ncbi Rapid neutrophil response controls fast-replicating intracellular bacteria but not slow-replicating Mycobacterium tuberculosis
    P Seiler
    Max Planck Institut für Infektionsbiologie, D 10117 Berlin, Germany
    J Infect Dis 181:671-80. 2000
  6. ncbi Variable immune response against a developmentally regulated self-antigen
    U Steinhoff
    Department of Immunology, Max Planck Institute for Infection Biology, Monbijoustrasse 2, Berlin, D 10117, Germany
    J Autoimmun 12:27-34. 1999
  7. ncbi Exacerbated colitis associated with elevated levels of activated CD4+ T cells in TCRalpha chain transgenic mice
    Immo Prinz
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany
    Gastroenterology 126:170-81. 2004
  8. ncbi TLR-activated B cells suppress T cell-mediated autoimmunity
    Vicky Lampropoulou
    Deutsches Rheuma ForschungsZentrum, Berlin, Germany
    J Immunol 180:4763-73. 2008
  9. ncbi Restricted expression of C-type lectin-like natural killer receptors by CD8 T cells in the murine small intestine
    Nathalie Jänner
    Department of Immunology, Max Planck Institute for Infection Biology, Chariteplatz, Berlin, Germany
    Immunology 125:38-47. 2008
  10. ncbi Proteasome-mediated degradation of IkappaBalpha and processing of p105 in Crohn disease and ulcerative colitis
    Alexander Visekruna
    Max Planck Institute of Infection Biology, Berlin, Germany
    J Clin Invest 116:3195-203. 2006

Collaborators

Detail Information

Publications17

  1. ncbi Altered intestinal immune system but normal antibacterial resistance in the absence of P-selectin and ICAM-1
    U Steinhoff
    Department of Immunology, Max Planck Institute of Infection Biology, Berlin, Germany
    J Immunol 160:6112-20. 1998
    ..These findings demonstrate that P-selectin and ICAM-1 are critically involved in the shaping of lymphocyte populations of the gut but have only a minor influence on systemic and regional host defense against intracellular bacteria...
  2. ncbi Who controls the crowd? New findings and old questions about the intestinal microflora
    Ulrich Steinhoff
    Max Planck Institute of Infection Biology, 10117 Berlin, Germany
    Immunol Lett 99:12-6. 2005
    ..This review discusses recent and old findings on function and immunological relevance of the endogenous microflora...
  3. ncbi Leprosy susceptibility-a matter of protein degradation? The role of proteasomes in infection and disease
    Ulrich Steinhoff
    Max Planck Institute of Infection Biology, Berlin, Germany
    Int J Lepr Other Mycobact Dis 73:135-7. 2005
  4. ncbi Autoimmune intestinal pathology induced by hsp60-specific CD8 T cells
    U Steinhoff
    Department of Immunology, Max Planck Institute of Infection Biology, Germany
    Immunity 11:349-58. 1999
    ..This report demonstrates that CD8 T cells with defined antigen specificity cause intestinal inflammation, emphasizing a link between infection and autoimmune disease...
  5. ncbi Rapid neutrophil response controls fast-replicating intracellular bacteria but not slow-replicating Mycobacterium tuberculosis
    P Seiler
    Max Planck Institut für Infektionsbiologie, D 10117 Berlin, Germany
    J Infect Dis 181:671-80. 2000
    ....
  6. ncbi Variable immune response against a developmentally regulated self-antigen
    U Steinhoff
    Department of Immunology, Max Planck Institute for Infection Biology, Monbijoustrasse 2, Berlin, D 10117, Germany
    J Autoimmun 12:27-34. 1999
    ..These findings suggest that in line 23 two different mechanisms regulated levels of the immune response: clonal reduction/deletion of VSV-G-specific T cells during early life followed by peripheral anergy at a later stage...
  7. ncbi Exacerbated colitis associated with elevated levels of activated CD4+ T cells in TCRalpha chain transgenic mice
    Immo Prinz
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany
    Gastroenterology 126:170-81. 2004
    ....
  8. ncbi TLR-activated B cells suppress T cell-mediated autoimmunity
    Vicky Lampropoulou
    Deutsches Rheuma ForschungsZentrum, Berlin, Germany
    J Immunol 180:4763-73. 2008
    ..Altogether, our data indicate that B cells link recognition of microbial products via TLR to suppression of a T cell-mediated autoimmune disease...
  9. ncbi Restricted expression of C-type lectin-like natural killer receptors by CD8 T cells in the murine small intestine
    Nathalie Jänner
    Department of Immunology, Max Planck Institute for Infection Biology, Chariteplatz, Berlin, Germany
    Immunology 125:38-47. 2008
    ....
  10. ncbi Proteasome-mediated degradation of IkappaBalpha and processing of p105 in Crohn disease and ulcerative colitis
    Alexander Visekruna
    Max Planck Institute of Infection Biology, Berlin, Germany
    J Clin Invest 116:3195-203. 2006
    ..These findings suggest that distinct proteasome subunits influence the intensity of NF-kappaB-mediated inflammation in IBD patients...
  11. ncbi Antitopes define preferential proteasomal cleavage site usage
    Britta Strehl
    Institut für Biochemie and Klinik für Kardiologie und Pulmologie, Charite Universitatsmedizin, and Max Planck Institut für Infektionsbiologie, Berlin, Germany
    J Biol Chem 283:17891-7. 2008
    ..This method is also applicable to other major histocompatibility class I epitopes as is shown for two potential epitopes derived from Coxsackievirus...
  12. ncbi Link between organ-specific antigen processing by 20S proteasomes and CD8(+) T cell-mediated autoimmunity
    Ulrike Kuckelkorn
    Institute of Biochemistry, Charite, Humboldt University, D-10117 Berlin, Germany
    J Exp Med 195:983-90. 2002
    ..We propose tissue-specific antigen processing by 20S proteasomes as a potential mechanism to control organ-specific immune responses...
  13. ncbi Promiscuous peptide recognition of an autoreactive CD8(+) T-cell clone is responsible for autoimmune intestinal pathology
    Immo Prinz
    Max Planck Institute for Infection Biology, Department of Immunology, Schumannstr 21 22, Campus Charite Mitte, D 10117 Berlin, Germany
    J Autoimmun 18:281-7. 2002
    ..Thus a single TCR is not only sufficient for crossrecognition with peptides that share minimal sequence homology, moreover this promiscuous TCR reactivity accounts also for immunopathology as recently shown...
  14. ncbi Syk tyrosine kinase participates in beta1-integrin signaling and inflammatory responses in airway epithelial cells
    Marina Ulanova
    Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
    Am J Physiol Lung Cell Mol Physiol 288:L497-507. 2005
    ..We propose that Syk is involved in signaling pathways induced by integrin engagement in airway EC. Syk-mediated signaling regulates IL-6 and ICAM-1 expression and may be important in the pathophysiology of lung inflammation...
  15. ncbi Differential expression of spleen tyrosine kinase Syk isoforms in tissues: Effects of the microbial flora
    Florentina Duta
    Department of Medicine, University of Alberta, Edmonton, AB, Canada
    Histochem Cell Biol 126:495-505. 2006
    ..In summary, our study reveals new and broad tissue expression of both Syk isoforms and demonstrates that lack of microbial flora results in selectively increased expression of Syk (S) isoform in lung and spleen...
  16. ncbi Poor correlation between BCG vaccination-induced T cell responses and protection against tuberculosis
    Hans Willi Mittrücker
    Department of Immunology, Max Planck Institute for Infection Biology, Caritéplatz 1, 10117 Berlin, Germany
    Proc Natl Acad Sci U S A 104:12434-9. 2007
    ..tuberculosis rather than the strength of protection. Our data question the measurement of IFN-gamma secretion by CD4(+) T cells and emphasize the need for new biomarkers for evaluation of tuberculosis vaccine efficacies...
  17. ncbi Immunoproteasomes are essential for clearance of Listeria monocytogenes in nonlymphoid tissues but not for induction of bacteria-specific CD8+ T cells
    Britta Strehl
    Institut fur Biochemie, Charite Universitatsmedizin, Berlin, Germany
    J Immunol 177:6238-44. 2006
    ..In summary, our studies demonstrate that induction of I-proteasomes is required for CD8(+) T cell-mediated elimination of L. monocytogenes from nonlymphoid but not lymphoid tissues...