| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
CUTTING EDGE |
* Institute of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms-Universität, Bonn, Germany;
Department of Nephrology and Clinical Immunology, University Hospital of the Rheinisch-Westfaelische Technische Hochschule, Aachen, Germany;
Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; and
Institute for Organic Chemistry, Eberhard Karls University, Tübingen, Germany
Cross-presentation of peripheral self-Ags by dendritic cells (DC) can induce deletion of autoreactive CTL by a mechanism termed cross-tolerance. Activation of DC by microbial TLR ligands is thought to result in adaptive immunity. However, activation of tolerogenic DC may cause autoimmunity by stimulating instead of deleting autoreactive CTL. To investigate this scenario, we have monitored the response of autoreactive CTL in specific for the transgenic self Ag, OVA, expressed in pancreatic islets of RIP-mOVA mice injected with ligands of TLR2, 3, 4, and 9. This somewhat enhanced proliferation and cytokine production, and moderately reduced the CTL number able to induce autoimmunity. Nevertheless, physiological CTL numbers were deleted before disease ensued, unless specific CD4 T cell help was provided. In conclusion, DC activation by TLR ligands was insufficient to break peripheral cross-tolerance in the absence of specific CD4 T cell help, and triggered autoimmunity by stimulating the early effector phase of autoreactive CTL only when their precursor frequency was extremely high.
This article has been cited by other articles:
|
|
 |
|
  R. Gorczynski, I. Khatri, L. Lee, and I. Boudakov An Interaction between CD200 and Monoclonal Antibody Agonists to CD200R2 in Development of Dendritic Cells That Preferentially Induce Populations of CD4+CD25+ T Regulatory Cells J. Immunol., May 1, 2008; 180(9): 5946 - 5955. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Lukacs-Kornek, S. Burgdorf, L. Diehl, S. Specht, M. Kornek, and C. Kurts The Kidney-Renal Lymph Node-System Contributes to Cross-Tolerance against Innocuous Circulating Antigen J. Immunol., January 15, 2008; 180(2): 706 - 715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. J. Singh, M. Cox, and R. H. Schwartz TLR Ligands Differentially Modulate T Cell Responses to Acute and Chronic Antigen Presentation J. Immunol., December 15, 2007; 179(12): 7999 - 8008. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. M. den Haan, G. Kraal, and M. J. Bevan Cutting Edge: Lipopolysaccharide Induces IL-10-Producing Regulatory CD4+ T Cells That Suppress the CD8+ T Cell Response J. Immunol., May 1, 2007; 178(9): 5429 - 5433. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Zipris, E. Lien, A. Nair, J. X. Xie, D. L. Greiner, J. P. Mordes, and A. A. Rossini TLR9-Signaling Pathways Are Involved in Kilham Rat Virus-Induced Autoimmune Diabetes in the Biobreeding Diabetes-Resistant Rat J. Immunol., January 15, 2007; 178(2): 693 - 701. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Martin-Orozco, Y.-H. Wang, H. Yagita, and C. Dong Cutting Edge: Programed Death (PD) Ligand-1/PD-1 Interaction Is Required for CD8+ T Cell Tolerance to Tissue Antigens J. Immunol., December 15, 2006; 177(12): 8291 - 8295. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. F. Roelofs, W. C. Boelens, L. A. B. Joosten, S. Abdollahi-Roodsaz, J. Geurts, L. U. Wunderink, B. W. Schreurs, W. B. van den Berg, and T. R. D. J. Radstake Identification of Small Heat Shock Protein B8 (HSP22) as a Novel TLR4 Ligand and Potential Involvement in the Pathogenesis of Rheumatoid Arthritis. J. Immunol., June 1, 2006; 176(11): 7021 - 7027. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. S. Fujinami, M. G. von Herrath, U. Christen, and J. L. Whitton Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease Clin. Microbiol. Rev., January 1, 2006; 19(1): 80 - 94. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
