The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes.
Toll-Like Receptors (TLR) are critical elements of the innate arm of the vertebrate immune system. They constitute a multigenic family of receptors which collectively bind a diverse array of--exogeneous as well as endogeneous--ligands. An exponential burst of knowledge has defined their biological r...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2009-11-01
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| Series: | PLoS ONE |
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19924287/?tool=EBI |
| _version_ | 1818394655081889792 |
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| author | Philippe Georgel Cécile Macquin Seiamak Bahram |
| author_facet | Philippe Georgel Cécile Macquin Seiamak Bahram |
| author_sort | Philippe Georgel |
| collection | DOAJ |
| description | Toll-Like Receptors (TLR) are critical elements of the innate arm of the vertebrate immune system. They constitute a multigenic family of receptors which collectively bind a diverse array of--exogeneous as well as endogeneous--ligands. An exponential burst of knowledge has defined their biological role in fight against infections and generation/modulation of auto-immune disorders. Hence, they could at least be conceptually recognized--despite being structurally unrelated - as innate counterparts to Major Histocompatibility Complex (MHC) molecules--equally recognizing antigenic ligands (albeit structurally more homogeneous i.e., peptides), again derived from self and/or non-self sources--preeminent this time in adaptive immunity. Our great disparities in face of infections and/or susceptibility to auto-immune diseases have provoked an intense search for genetic explanations, in part satisfied by the extraordinary MHC allelic repertoire. An equally in-depth and systematic analysis of TLR diversity is lacking despite numerous independent reports of a growing number of SNPs within these loci. The work described here aims at providing a preliminary picture of the allelic repertoire--and not purely SNPs--of all 10 human TLR coding sequences (with exception of TLR3) within a single cohort of up to 100 individuals. It appears from our work that TLR are unequally polymorphic: TLR2 (DNA alleles: 7/protein alleles: 3), 4 (4/3), 7 (6/3), 8 (9/2) and 9 (8/3) being comparatively least diverse whereas TLR1 (11/10), 5 (14/12), 6 (10/8) and 10 (15/10) show a substantial number of alleles. In addition to allelic assignment of a large number of SNPs, 10 new polymorphic positions were hereby identified. Hence this work depicts a first overview of the diversity of almost all human TLR genes, a prelude for large-scale population genetics as well as genetic association studies. |
| first_indexed | 2024-12-14T06:04:39Z |
| format | Article |
| id | doaj.art-71147f1bd5024901abbf237d30068a17 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-14T06:04:39Z |
| publishDate | 2009-11-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-71147f1bd5024901abbf237d30068a172022-12-21T23:14:19ZengPublic Library of Science (PLoS)PLoS ONE1932-62032009-11-01411e780310.1371/journal.pone.0007803The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes.Philippe GeorgelCécile MacquinSeiamak BahramToll-Like Receptors (TLR) are critical elements of the innate arm of the vertebrate immune system. They constitute a multigenic family of receptors which collectively bind a diverse array of--exogeneous as well as endogeneous--ligands. An exponential burst of knowledge has defined their biological role in fight against infections and generation/modulation of auto-immune disorders. Hence, they could at least be conceptually recognized--despite being structurally unrelated - as innate counterparts to Major Histocompatibility Complex (MHC) molecules--equally recognizing antigenic ligands (albeit structurally more homogeneous i.e., peptides), again derived from self and/or non-self sources--preeminent this time in adaptive immunity. Our great disparities in face of infections and/or susceptibility to auto-immune diseases have provoked an intense search for genetic explanations, in part satisfied by the extraordinary MHC allelic repertoire. An equally in-depth and systematic analysis of TLR diversity is lacking despite numerous independent reports of a growing number of SNPs within these loci. The work described here aims at providing a preliminary picture of the allelic repertoire--and not purely SNPs--of all 10 human TLR coding sequences (with exception of TLR3) within a single cohort of up to 100 individuals. It appears from our work that TLR are unequally polymorphic: TLR2 (DNA alleles: 7/protein alleles: 3), 4 (4/3), 7 (6/3), 8 (9/2) and 9 (8/3) being comparatively least diverse whereas TLR1 (11/10), 5 (14/12), 6 (10/8) and 10 (15/10) show a substantial number of alleles. In addition to allelic assignment of a large number of SNPs, 10 new polymorphic positions were hereby identified. Hence this work depicts a first overview of the diversity of almost all human TLR genes, a prelude for large-scale population genetics as well as genetic association studies.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19924287/?tool=EBI |
| spellingShingle | Philippe Georgel Cécile Macquin Seiamak Bahram The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. PLoS ONE |
| title | The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. |
| title_full | The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. |
| title_fullStr | The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. |
| title_full_unstemmed | The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. |
| title_short | The heterogeneous allelic repertoire of human toll-like receptor (TLR) genes. |
| title_sort | heterogeneous allelic repertoire of human toll like receptor tlr genes |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19924287/?tool=EBI |
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