Heat Shock Proteins: Potent Mediators of Inflammation and Immunity /
| Autor Corporativo: | |
|---|---|
| Otros Autores: | , |
| Formato: | eBook |
| Lenguaje: | English |
| Publicado: |
Dordrecht :
Springer Netherlands : Imprint: Springer,
2007.
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| Edición: | 1st ed. 2007. |
| Colección: | Heat Shock Proteins,
1 |
| Materias: |
Tabla de Contenidos:
- Mechanisms of Heat Shock Protein Release
- Release of Heat Shock Proteins: Passive Versus Active Release Mechanisms
- Hsp70 Peptide Acting as a Danger Signal for Natural Killer (NK) Cells
- Mechanisms of Stress-Induced Cellular Hsp72 Release
- Roles of Extracellular Heat Shock Proteins: A New Sense of Danger
- Heat Shock Protein Binding and Receptor-Mediated Signaling
- Macrophages and the Stress Response
- Heat Shock Proteins and Scavenger Receptors
- The Inside Story: Anti-Inflammatory roles of HSF1 and heat shock proteins
- Interaction of Heat Shock Protein 60 with Innate Immune Cells
- Immune Responses Elicited by Heat Shock Proteins
- HSP-APC Interactions: Initiation of Immune Responses
- Extracellular Functions for an Intracellular Protein: GRP94/GP96 Interactions with the Mammalian Immune System
- Hsp-Induced Stimulation of Immune Responses
- The Role of Heat Shock Proteins in the Elicitation of Immune Responses
- Hsp70 Family Members, Danger Signals and Autoimmunity
- The Immune Response Under Stress: Class I HLA Presentation of Host-Derived Peptides
- Extracellular Hsp 72: A Double-Edged Sword for Host Defense
- HSP60: A Pleiotropic Immune Signal
- Antigen Processing, Presentation and Effect on Inflammation and Disease
- Impact of HSP-Chaperoned Peptides on the MHC Class II-Dependent Presentation and Activation of CD4+ T Cells in Regard of Allo- and Autoantigens
- Heat Shock Proteins are Targets for T Cell Regulation: How Microbial HSP Induce IL10 Producing Anti-Inflammatory T Cells
- The Pro- and Anti-Inflammatory Properties of the Stress Protein GP96
- Anti-Tumor Response and Heat Shock Proteins (HSP): A friend or Foe relationship?
- Heat Shock Proteins and the Resolution of Inflammation by Lymphocytes.