Ebook: Toll-like Receptors in Inflammation
- Tags: Immunology, Infectious Diseases, Medical Microbiology, Cell Biology, Pharmacology/Toxicology
- Series: Progress in Inflammation Research
- Year: 2005
- Publisher: Birkhäuser Basel
- Edition: 1
- Language: English
- pdf
Toll-like receptors (TLRs) are critical mediators of the innate immune response in mammals. This family of receptors recognizes a variety of microbial products or motifs and initiates the host response to infection. Examples include TLR4 which recognizes lipopolysaccharide (LPS) from Gram-negative bacteria, TLR3 which recognizes viral double-stranded RNA, and TLR9 which recognizes CpG DNA motifs, found in both viruses and bacteria. All TLRs possess an intracellular region termed the Toll-IL-1 receptor-Resistance (TIR) domain which is essential for signaling from these receptors. The specificity of signaling from individual TLRs arises from differential utilization of adapter proteins. This specificity results in a tailoring of the host defense response depending on the microbe being sensed. TLRs are increasingly being implicated in both infectious and inflammatory diseases, notable examples being sepsis, inflammatory bowel disease, atherosclerosis, and asthma. There is, therefore, great interest in targeting TLRs therapeutically since a disruption of TLR function will result in a decrease in the production of inflammatory mediators. This volume covers our current understanding of TLRs and their role in inflammation. Given the importance of TLRs in the inflammatory process and their emerging role in inflammatory diseases the book is of great interest to researchers working in inflammation and immunology.
Toll-like receptors (TLRs) are critical mediators of the innate immune response in mammals. This family of receptors recognizes a variety of microbial products or motifs and initiates the host response to infection. Examples include TLR4 which recognizes lipopolysaccharide (LPS) from Gram-negative bacteria, TLR3 which recognizes viral double-stranded RNA, and TLR9 which recognizes CpG DNA motifs, found in both viruses and bacteria. All TLRs possess an intracellular region termed the Toll-IL-1 receptor-Resistance (TIR) domain which is essential for signaling from these receptors. The specificity of signaling from individual TLRs arises from differential utilization of adapter proteins. This specificity results in a tailoring of the host defense response depending on the microbe being sensed. TLRs are increasingly being implicated in both infectious and inflammatory diseases, notable examples being sepsis, inflammatory bowel disease, atherosclerosis, and asthma. There is, therefore, great interest in targeting TLRs therapeutically since a disruption of TLR function will result in a decrease in the production of inflammatory mediators. This volume covers our current understanding of TLRs and their role in inflammation. Given the importance of TLRs in the inflammatory process and their emerging role in inflammatory diseases the book is of great interest to researchers working in inflammation and immunology.
Toll-like receptors (TLRs) are critical mediators of the innate immune response in mammals. This family of receptors recognizes a variety of microbial products or motifs and initiates the host response to infection. Examples include TLR4 which recognizes lipopolysaccharide (LPS) from Gram-negative bacteria, TLR3 which recognizes viral double-stranded RNA, and TLR9 which recognizes CpG DNA motifs, found in both viruses and bacteria. All TLRs possess an intracellular region termed the Toll-IL-1 receptor-Resistance (TIR) domain which is essential for signaling from these receptors. The specificity of signaling from individual TLRs arises from differential utilization of adapter proteins. This specificity results in a tailoring of the host defense response depending on the microbe being sensed. TLRs are increasingly being implicated in both infectious and inflammatory diseases, notable examples being sepsis, inflammatory bowel disease, atherosclerosis, and asthma. There is, therefore, great interest in targeting TLRs therapeutically since a disruption of TLR function will result in a decrease in the production of inflammatory mediators. This volume covers our current understanding of TLRs and their role in inflammation. Given the importance of TLRs in the inflammatory process and their emerging role in inflammatory diseases the book is of great interest to researchers working in inflammation and immunology.
Content:
Front Matter....Pages i-xii
TLRs as bacterial sensors....Pages 1-17
Toll-like receptors and rheumatoid arthritis: is there a connection?....Pages 19-40
Toll-like receptor 9 and systemic autoimmune diseases....Pages 41-61
Toll-like receptors and airway disease....Pages 63-86
Toll-like receptors and vascular disease....Pages 87-106
Toll-like receptors and inflammatory bowel disease....Pages 107-123
Toll-like receptor signaling in the liver....Pages 125-142
Toll-like receptors as key sensors of viral infection....Pages 143-171
IRAK-4: A key kinase involved in toll-like receptor signaling and resistance to bacterial infection....Pages 173-192
Endogenous regulation of toll-like receptor signalling....Pages 193-211
Tuning of inflammatory cytokines and toll-like receptors by TIR8/SIGIRR, a member of the IL-1 receptor family with unique structure and regulation....Pages 213-222
Toll-like receptors as pharmacological targets....Pages 223-240
Back Matter....Pages 241-246
Toll-like receptors (TLRs) are critical mediators of the innate immune response in mammals. This family of receptors recognizes a variety of microbial products or motifs and initiates the host response to infection. Examples include TLR4 which recognizes lipopolysaccharide (LPS) from Gram-negative bacteria, TLR3 which recognizes viral double-stranded RNA, and TLR9 which recognizes CpG DNA motifs, found in both viruses and bacteria. All TLRs possess an intracellular region termed the Toll-IL-1 receptor-Resistance (TIR) domain which is essential for signaling from these receptors. The specificity of signaling from individual TLRs arises from differential utilization of adapter proteins. This specificity results in a tailoring of the host defense response depending on the microbe being sensed. TLRs are increasingly being implicated in both infectious and inflammatory diseases, notable examples being sepsis, inflammatory bowel disease, atherosclerosis, and asthma. There is, therefore, great interest in targeting TLRs therapeutically since a disruption of TLR function will result in a decrease in the production of inflammatory mediators. This volume covers our current understanding of TLRs and their role in inflammation. Given the importance of TLRs in the inflammatory process and their emerging role in inflammatory diseases the book is of great interest to researchers working in inflammation and immunology.
Content:
Front Matter....Pages i-xii
TLRs as bacterial sensors....Pages 1-17
Toll-like receptors and rheumatoid arthritis: is there a connection?....Pages 19-40
Toll-like receptor 9 and systemic autoimmune diseases....Pages 41-61
Toll-like receptors and airway disease....Pages 63-86
Toll-like receptors and vascular disease....Pages 87-106
Toll-like receptors and inflammatory bowel disease....Pages 107-123
Toll-like receptor signaling in the liver....Pages 125-142
Toll-like receptors as key sensors of viral infection....Pages 143-171
IRAK-4: A key kinase involved in toll-like receptor signaling and resistance to bacterial infection....Pages 173-192
Endogenous regulation of toll-like receptor signalling....Pages 193-211
Tuning of inflammatory cytokines and toll-like receptors by TIR8/SIGIRR, a member of the IL-1 receptor family with unique structure and regulation....Pages 213-222
Toll-like receptors as pharmacological targets....Pages 223-240
Back Matter....Pages 241-246
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