A common human TLR1 polymorphism regulates the innate immune response to lipopeptides
Toll‐like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses t...
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Published in | European Journal of Immunology Vol. 37; no. 8; pp. 2280 - 2289 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Weinheim
WILEY‐VCH Verlag
01.08.2007
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Subjects | |
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Abstract | Toll‐like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses through TLR1/2 or TLR2/6 heterodimers. It is not currently known whether polymorphisms in TLR1 regulate the innate immune response. We stimulated human whole blood with triacylated lipopeptide, a ligand for TLR1/2 heterodimers, and found substantial inter‐individual variation in the immune response. We sequenced the coding region of TLR1 and found a non‐synonymous polymorphism, I602S (base pair T1805G), that regulated signalling. In comparison to TLR1_602S, the 602I variant mediated substantially greater basal and lipopeptide‐induced NF‐κB signalling in transfected HEK293 cells. These signalling differences among TLR1 variants were also found with stimulation by extracts of Mycobacterium tuberculosis. Furthermore, individuals with the 602II genotype produced substantially more IL‐6 than those with the 602SS variant in a lipopeptide‐stimulated whole‐blood cytokine assay. Together, these observations demonstrate that variation in the inflammatory response to bacterial lipopeptides is regulated by a common TLR1 transmembrane domain polymorphism that could potentially impact the innate immune response and clinical susceptibility to a wide spectrum of pathogens.
See accompanying article: http://dx.doi.org/10.1002/eji.200737604 |
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AbstractList | Toll‐like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses through TLR1/2 or TLR2/6 heterodimers. It is not currently known whether polymorphisms in TLR1 regulate the innate immune response. We stimulated human whole blood with triacylated lipopeptide, a ligand for TLR1/2 heterodimers, and found substantial inter‐individual variation in the immune response. We sequenced the coding region of TLR1 and found a non‐synonymous polymorphism, I602S (base pair T1805G), that regulated signalling. In comparison to TLR1_602S, the 602I variant mediated substantially greater basal and lipopeptide‐induced NF‐κB signalling in transfected HEK293 cells. These signalling differences among TLR1 variants were also found with stimulation by extracts of Mycobacterium tuberculosis. Furthermore, individuals with the 602II genotype produced substantially more IL‐6 than those with the 602SS variant in a lipopeptide‐stimulated whole‐blood cytokine assay. Together, these observations demonstrate that variation in the inflammatory response to bacterial lipopeptides is regulated by a common TLR1 transmembrane domain polymorphism that could potentially impact the innate immune response and clinical susceptibility to a wide spectrum of pathogens.
See accompanying article: http://dx.doi.org/10.1002/eji.200737604 Toll-like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses through TLR1/2 or TLR2/6 heterodimers. It is not currently known whether polymorphisms in TLR1 regulate the innate immune response. We stimulated human whole blood with triacylated lipopeptide, a ligand for TLR1/2 heterodimers, and found substantial inter-individual variation in the immune response. We sequenced the coding region of TLR1 and found a non-synonymous polymorphism, I602S (base pair T1805G), that regulated signalling. In comparison to TLR1_602S, the 602I variant mediated substantially greater basal and lipopeptide-induced NF-kappaB signalling in transfected HEK293 cells. These signalling differences among TLR1 variants were also found with stimulation by extracts of Mycobacterium tuberculosis. Furthermore, individuals with the 602II genotype produced substantially more IL-6 than those with the 602SS variant in a lipopeptide-stimulated whole-blood cytokine assay. Together, these observations demonstrate that variation in the inflammatory response to bacterial lipopeptides is regulated by a common TLR1 transmembrane domain polymorphism that could potentially impact the innate immune response and clinical susceptibility to a wide spectrum of pathogens. Toll-like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses through TLR1/2 or TLR2/6 heterodimers. It is not currently known whether polymorphisms in TLR1 regulate the innate immune response. We stimulated human whole blood with triacylated lipopeptide, a ligand for TLR1/2 heterodimers, and found substantial inter-individual variation in the immune response. We sequenced the coding region of TLR1 and found a non-synonymous polymorphism, I602S (base pair T1805G), that regulated signalling. In comparison to TLR1_602S, the 602I variant mediated substantially greater basal and lipopeptide-induced NF-B signalling in transfected HEK293 cells. These signalling differences among TLR1 variants were also found with stimulation by extracts of Mycobacterium tuberculosis. Furthermore, individuals with the 602II genotype produced substantially more IL-6 than those with the 602SS variant in a lipopeptide-stimulated whole-blood cytokine assay. Together, these observations demonstrate that variation in the inflammatory response to bacterial lipopeptides is regulated by a common TLR1 transmembrane domain polymorphism that could potentially impact the innate immune response and clinical susceptibility to a wide spectrum of pathogens. See accompanying article: http://dx.doi.org/10.1002/eji.200737604 . Toll‐like receptors (TLR) are critical mediators of the immune response to pathogens and human polymorphisms in this gene family regulate inflammatory pathways and are associated with susceptibility to infection. Lipopeptides are present in a wide variety of microbes and stimulate immune responses through TLR1/2 or TLR2/6 heterodimers. It is not currently known whether polymorphisms in TLR1 regulate the innate immune response. We stimulated human whole blood with triacylated lipopeptide, a ligand for TLR1/2 heterodimers, and found substantial inter‐individual variation in the immune response. We sequenced the coding region of TLR1 and found a non‐synonymous polymorphism, I602S (base pair T1805G), that regulated signalling. In comparison to TLR1_602S, the 602I variant mediated substantially greater basal and lipopeptide‐induced NF‐κB signalling in transfected HEK293 cells. These signalling differences among TLR1 variants were also found with stimulation by extracts of Mycobacterium tuberculosis . Furthermore, individuals with the 602II genotype produced substantially more IL‐6 than those with the 602SS variant in a lipopeptide‐stimulated whole‐blood cytokine assay. Together, these observations demonstrate that variation in the inflammatory response to bacterial lipopeptides is regulated by a common TLR1 transmembrane domain polymorphism that could potentially impact the innate immune response and clinical susceptibility to a wide spectrum of pathogens. See accompanying article: http://dx.doi.org/10.1002/eji.200737604 |
Author | Dunstan, Sarah J. Chau, Tran T. H. Lan, Nguyen T. N. Hawn, Thomas R. Nachman, Alex Hien, Tran T. Misch, E. Ann Farrar, Jeremy J. Rodrigues, Stephanie Quy, Hoang T. Thwaites, Guy E. Janer, Marta Aderem, Alan |
Author_xml | – sequence: 1 givenname: Thomas R. surname: Hawn fullname: Hawn, Thomas R. email: thawn@u.washington.edu – sequence: 2 givenname: E. Ann surname: Misch fullname: Misch, E. Ann – sequence: 3 givenname: Sarah J. surname: Dunstan fullname: Dunstan, Sarah J. – sequence: 4 givenname: Guy E. surname: Thwaites fullname: Thwaites, Guy E. – sequence: 5 givenname: Nguyen T. N. surname: Lan fullname: Lan, Nguyen T. N. – sequence: 6 givenname: Hoang T. surname: Quy fullname: Quy, Hoang T. – sequence: 7 givenname: Tran T. H. surname: Chau fullname: Chau, Tran T. H. – sequence: 8 givenname: Stephanie surname: Rodrigues fullname: Rodrigues, Stephanie – sequence: 9 givenname: Alex surname: Nachman fullname: Nachman, Alex – sequence: 10 givenname: Marta surname: Janer fullname: Janer, Marta – sequence: 11 givenname: Tran T. surname: Hien fullname: Hien, Tran T. – sequence: 12 givenname: Jeremy J. surname: Farrar fullname: Farrar, Jeremy J. – sequence: 13 givenname: Alan surname: Aderem fullname: Aderem, Alan |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17595679$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Bacterial Proteins - immunology Base Sequence Fluorescent Antibody Technique Genetics Humans Immunity, Innate Immunoblotting Infectious diseases Inflammation Innate immunity Lipoproteins - immunology Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology NF-kappa B Polymerase Chain Reaction Polymorphism, Single Nucleotide Toll-Like Receptor 1 - genetics Transfection |
Title | A common human TLR1 polymorphism regulates the innate immune response to lipopeptides |
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