000 03881nam a22005415i 4500
001 978-3-7643-7441-9
003 DE-He213
005 20161121230710.0
007 cr nn 008mamaa
008 100301s2005 sz | s |||| 0|eng d
020 _a9783764374419
_9978-3-7643-7441-9
024 7 _a10.1007/3-7643-7441-1
_2doi
050 4 _aQR180-189.5
072 7 _aMJCM
_2bicssc
072 7 _aMED044000
_2bisacsh
082 0 4 _a616.079
_223
245 1 0 _aToll-like Receptors in Inflammation
_h[electronic resource] /
_cedited by Luke A.J. O’Neill, Elizabeth Brint.
264 1 _aBasel :
_bBirkhäuser Basel,
_c2005.
300 _aXII, 246 p.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
490 1 _aProgress in Inflammation Research
505 0 _aTLRs as bacterial sensors -- Toll-like receptors and rheumatoid arthritis: is there a connection? -- Toll-like receptor 9 and systemic autoimmune diseases -- Toll-like receptors and airway disease -- Toll-like receptors and vascular disease -- Toll-like receptors and inflammatory bowel disease -- Toll-like receptor signaling in the liver -- Toll-like receptors as key sensors of viral infection -- IRAK-4: A key kinase involved in toll-like receptor signaling and resistance to bacterial infection -- Endogenous regulation of toll-like receptor signalling -- Tuning of inflammatory cytokines and toll-like receptors by TIR8/SIGIRR, a member of the IL-1 receptor family with unique structure and regulation -- Toll-like receptors as pharmacological targets.
520 _aToll-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.
650 0 _aMedicine.
650 0 _aImmunology.
650 0 _aMedical microbiology.
650 0 _aPharmacology.
650 0 _aInfectious diseases.
650 0 _aCell biology.
650 1 4 _aBiomedicine.
650 2 4 _aImmunology.
650 2 4 _aInfectious Diseases.
650 2 4 _aMedical Microbiology.
650 2 4 _aCell Biology.
650 2 4 _aPharmacology/Toxicology.
700 1 _aO’Neill, Luke A.J.
_eeditor.
700 1 _aBrint, Elizabeth.
_eeditor.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9783764372859
830 0 _aProgress in Inflammation Research
856 4 0 _uhttp://dx.doi.org/10.1007/3-7643-7441-1
912 _aZDB-2-SBL
950 _aBiomedical and Life Sciences (Springer-11642)
999 _c502639
_d502639