Cutting Edge: Heat Shock Protein 60 Is a Putative Endogenous Ligand of the Toll-Like Receptor-4 Complex1
- K. Ohashi, V. Burkart, S. Flohé, H. Kolb
- BiologyJournal of Immunology
- 15 January 2000
It is reported here that macrophages of C3H/HeJ mice, carrying a mutant Toll-like-receptor (Tlr) 4 are nonresponsive to hsp60, and this is the first report of a putative endogenous ligand of the Tlr4 complex.
Human 60-kDa heat-shock protein: a danger signal to the innate immune system.
- W. Chen, U. Syldath, K. Bellmann, V. Burkart, H. Kolb
- Biology, MedicineJournal of Immunology
- 15 March 1999
It is shown that autologous hsp60 is also an Ag recognized by cells of the innate immune system, such as macrophages, and induces gene expression of the Th1-promoting cytokines IL-12 and IL-15.
Structural basis for ON-and OFF-center responses in retinal ganglion cells.
- E. V. Famiglietti, H. Kolb
- BiologyScience
- 8 October 1976
Comparison of dendritic field diameters and receptive fiedl center sizes of large ganglion cells suggests that neural circuitry in sublamina a conveys "OFF"-center properties and connections insublamina b "ON"- center properties to retinal ganglions.
Human Heat Shock Protein 60 Induces Maturation of Dendritic Cells Versus a Th1-Promoting Phenotype1
- S. Flohé, Jutta Brüggemann, H. Kolb
- BiologyJournal of Immunology
- 1 March 2003
HSP60 was found to rapidly activate the mitogen-activated protein kinases p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase as well as IκB in DC and stimulates DC more rapidly than LPS and elicits a Th1-promoting phenotype.
Mouse models of insulin dependent diabetes: low-dose streptozocin-induced diabetes and nonobese diabetic (NOD) mice.
- H. Kolb
- MedicineDiabetes Metabolism Reviews
- 1 July 1987
The Receptor for Heat Shock Protein 60 on Macrophages Is Saturable, Specific, and Distinct from Receptors for Other Heat Shock Proteins1
- C. Habich, K. Baumgart, H. Kolb, V. Burkart
- BiologyJournal of Immunology
- 15 January 2002
It is demonstrated for the first time that hsp60 binding to macrophages occurred at submicromolar concentrations, is saturable, and can be competed by unlabeled hSp60, but not by unrelated proteins, thus confirming the classic characteristics of specific ligand-receptor interactions.
Cholera Toxin B Pretreatment of Macrophages and Monocytes Diminishes Their Proinflammatory Responsiveness to Lipopolysaccharide1
- V. Burkart, Yoong-Eun Kim, H. Kolb
- Biology, MedicineJournal of Immunology
- 15 February 2002
In contrast to desensitization by low doses of LPS, tolerance induction by CTB occurred silently, i.e., in the absence of a measurable proinflammatory response, which may be relevant to the use of CTB in modulating immune-mediated diseases.
Nitric oxide: a pathogenetic factor in autoimmunity.
- H. Kolb, V. Kolb‐Bachofen
- Biology, MedicineImmunology today (Amsterdam. Regular ed.)
- 1992
Mice lacking the poly(ADP-ribose) polymerase gene are resistant to pancreatic beta-cell destruction and diabetes development induced by streptozocin
- V. Burkart, Zhao-Qi Wang, H. Kolb
- Biology, MedicineNature Network Boston
- 1 March 1999
This work shows that mice with a disrupted gene coding for poly (ADP-ribose) polymerase (PARP–/– mice) are completely resistant to the development of diabetes induced by the beta-cell toxin streptozocin, identifying NAD+ depletion caused by PARP activation as the dominant metabolic event in islet-cell destruction.
Active stage of autoimmune diabetes is associated with the expression of a novel cytokine, IGIF, which is located near Idd2.
- H. Rothe, N. Jenkins, N. Copeland, H. Kolb
- Biology, MedicineJournal of Clinical Investigation
- 1 February 1997
It is concluded that IGIF expression is abnormally regulated in autoimmune NOD mice and closely associated with diabetes development.
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