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Toll‐like receptor polymorphism in host immune response to infectious diseases: A review
Immunopolymorphism is considered as an important aspect behind the resistance or susceptibility of the host to an infectious disease. Over the years, researchers have explored many genetic factors for their role in immune surveillance against infectious diseases. Polymorphic characters in the gene e...
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Published in: | Scandinavian journal of immunology 2019-07, Vol.90 (1), p.e12771-n/a |
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description | Immunopolymorphism is considered as an important aspect behind the resistance or susceptibility of the host to an infectious disease. Over the years, researchers have explored many genetic factors for their role in immune surveillance against infectious diseases. Polymorphic characters in the gene encoding Toll‐like receptors (TLRs) play profound roles in inducing differential immune responses by the host against parasitic infections. Protein(s) encoded by TLR gene(s) are immensely important due to their ability of recognizing different types of pathogen associated molecular patterns (PAMPs). This study reviews the polymorphic residues present in the nucleotide or in the amino acid sequence of TLRs and their influence on alteration of inflammatory signalling pathways promoting either susceptibility or resistance to major infectious diseases, including tuberculosis, leishmaniasis, malaria and filariasis. Population‐based studies exploring TLR polymorphisms in humans are primarily emphasized to discuss the association of the polymorphic residues with the occurrence and epidemiology of the mentioned infectious diseases. Principal polymorphic residues in TLRs influencing immunity to infection are mostly single nucleotide polymorphisms (SNPs). I602S (TLR1), R677W (TLR2), P554S (TLR3), D299G (TLR4), F616L (TLR5), S249P (TLR6), Q11L (TLR7), M1V (TLR8), G1174A (TLR9) and G1031T (TLR10) are presented as the major influential SNPs in shaping immunity to pathogenic infections. The contribution of these SNPs in the structure‐function relationship of TLRs is yet not clear. Therefore, molecular studies on such polymorphisms can improve our understanding on the genetic basis of the immune response and pave the way for therapeutic intervention in a more feasible way. |
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Over the years, researchers have explored many genetic factors for their role in immune surveillance against infectious diseases. Polymorphic characters in the gene encoding Toll‐like receptors (TLRs) play profound roles in inducing differential immune responses by the host against parasitic infections. Protein(s) encoded by TLR gene(s) are immensely important due to their ability of recognizing different types of pathogen associated molecular patterns (PAMPs). This study reviews the polymorphic residues present in the nucleotide or in the amino acid sequence of TLRs and their influence on alteration of inflammatory signalling pathways promoting either susceptibility or resistance to major infectious diseases, including tuberculosis, leishmaniasis, malaria and filariasis. Population‐based studies exploring TLR polymorphisms in humans are primarily emphasized to discuss the association of the polymorphic residues with the occurrence and epidemiology of the mentioned infectious diseases. Principal polymorphic residues in TLRs influencing immunity to infection are mostly single nucleotide polymorphisms (SNPs). I602S (TLR1), R677W (TLR2), P554S (TLR3), D299G (TLR4), F616L (TLR5), S249P (TLR6), Q11L (TLR7), M1V (TLR8), G1174A (TLR9) and G1031T (TLR10) are presented as the major influential SNPs in shaping immunity to pathogenic infections. The contribution of these SNPs in the structure‐function relationship of TLRs is yet not clear. 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Over the years, researchers have explored many genetic factors for their role in immune surveillance against infectious diseases. Polymorphic characters in the gene encoding Toll‐like receptors (TLRs) play profound roles in inducing differential immune responses by the host against parasitic infections. Protein(s) encoded by TLR gene(s) are immensely important due to their ability of recognizing different types of pathogen associated molecular patterns (PAMPs). This study reviews the polymorphic residues present in the nucleotide or in the amino acid sequence of TLRs and their influence on alteration of inflammatory signalling pathways promoting either susceptibility or resistance to major infectious diseases, including tuberculosis, leishmaniasis, malaria and filariasis. Population‐based studies exploring TLR polymorphisms in humans are primarily emphasized to discuss the association of the polymorphic residues with the occurrence and epidemiology of the mentioned infectious diseases. Principal polymorphic residues in TLRs influencing immunity to infection are mostly single nucleotide polymorphisms (SNPs). I602S (TLR1), R677W (TLR2), P554S (TLR3), D299G (TLR4), F616L (TLR5), S249P (TLR6), Q11L (TLR7), M1V (TLR8), G1174A (TLR9) and G1031T (TLR10) are presented as the major influential SNPs in shaping immunity to pathogenic infections. The contribution of these SNPs in the structure‐function relationship of TLRs is yet not clear. Therefore, molecular studies on such polymorphisms can improve our understanding on the genetic basis of the immune response and pave the way for therapeutic intervention in a more feasible way.</description><subject>Amino acid sequence</subject><subject>Epidemiology</subject><subject>Filariasis</subject><subject>Genetic factors</subject><subject>Immune response</subject><subject>Immunosurveillance</subject><subject>Infections</subject><subject>infectious disease</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Leishmaniasis</subject><subject>Malaria</subject><subject>Parasitic diseases</subject><subject>pathogen‐associated molecular pattern</subject><subject>polymorphism</subject><subject>Population studies</subject><subject>Residues</subject><subject>resistance</subject><subject>Signal transduction</subject><subject>Single-nucleotide polymorphism</subject><subject>Structure-function relationships</subject><subject>susceptibility</subject><subject>TLR1 protein</subject><subject>TLR2 protein</subject><subject>TLR3 protein</subject><subject>TLR4 protein</subject><subject>TLR5 protein</subject><subject>TLR7 protein</subject><subject>TLR9 protein</subject><subject>Toll-like receptors</subject><subject>toll‐like receptor</subject><subject>Tropical diseases</subject><subject>Tuberculosis</subject><subject>Vector-borne diseases</subject><issn>0300-9475</issn><issn>1365-3083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp10L1OwzAUBWALgWgpDLwAssQCQ1o7jpuYrar4KarEQFlYosS5UV2SONgJVTcegWfkSXBJYUDCsuTBn46vD0KnlAypWyO7UkPqhyHdQ33KxtxjJGL7qE8YIZ4IQt5DR9auCKHMD9kh6jFKeED5uI-eF7ooPt8_CvUC2ICEutEG17rYlNrUS2VLrCq81LbBqizbaotsrSsLuNHuKgfZKN1anCkLiQV7hSeOvClYH6ODPCksnOzOAXq6uV5M77z5w-1sOpl7kkUR9Tj3Oc_cFmlGx2mQAM8jQYIoyqnPciFYFmaSkSwVARXukrE0pxBEICNJkpQN0EWXWxv92oJt4lJZCUWRVOAmi33fF777eEAcPf9DV7o1lZvOqYCFwr0onLrslDTaWgN5XBtVJmYTUxJvC49d4fF34c6e7RLbtITsV_407MCoA2tVwOb_pPjxftZFfgE4WosN</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Mukherjee, Suprabhat</creator><creator>Huda, Sahel</creator><creator>Sinha Babu, Santi P.</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7441-6426</orcidid></search><sort><creationdate>201907</creationdate><title>Toll‐like receptor polymorphism in host immune response to infectious diseases: A review</title><author>Mukherjee, Suprabhat ; Huda, Sahel ; Sinha Babu, Santi P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3881-55255d55d9bd16b4ae5f890488f123f993d7dc30db9419e5f33bf1e48ec8c0ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Amino acid sequence</topic><topic>Epidemiology</topic><topic>Filariasis</topic><topic>Genetic factors</topic><topic>Immune response</topic><topic>Immunosurveillance</topic><topic>Infections</topic><topic>infectious disease</topic><topic>Infectious diseases</topic><topic>Inflammation</topic><topic>Leishmaniasis</topic><topic>Malaria</topic><topic>Parasitic diseases</topic><topic>pathogen‐associated molecular pattern</topic><topic>polymorphism</topic><topic>Population studies</topic><topic>Residues</topic><topic>resistance</topic><topic>Signal transduction</topic><topic>Single-nucleotide polymorphism</topic><topic>Structure-function relationships</topic><topic>susceptibility</topic><topic>TLR1 protein</topic><topic>TLR2 protein</topic><topic>TLR3 protein</topic><topic>TLR4 protein</topic><topic>TLR5 protein</topic><topic>TLR7 protein</topic><topic>TLR9 protein</topic><topic>Toll-like receptors</topic><topic>toll‐like receptor</topic><topic>Tropical diseases</topic><topic>Tuberculosis</topic><topic>Vector-borne diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mukherjee, Suprabhat</creatorcontrib><creatorcontrib>Huda, Sahel</creatorcontrib><creatorcontrib>Sinha Babu, Santi P.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Scandinavian journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mukherjee, Suprabhat</au><au>Huda, Sahel</au><au>Sinha Babu, Santi P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toll‐like receptor polymorphism in host immune response to infectious diseases: A review</atitle><jtitle>Scandinavian journal of immunology</jtitle><addtitle>Scand J Immunol</addtitle><date>2019-07</date><risdate>2019</risdate><volume>90</volume><issue>1</issue><spage>e12771</spage><epage>n/a</epage><pages>e12771-n/a</pages><issn>0300-9475</issn><eissn>1365-3083</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>Immunopolymorphism is considered as an important aspect behind the resistance or susceptibility of the host to an infectious disease. Over the years, researchers have explored many genetic factors for their role in immune surveillance against infectious diseases. Polymorphic characters in the gene encoding Toll‐like receptors (TLRs) play profound roles in inducing differential immune responses by the host against parasitic infections. Protein(s) encoded by TLR gene(s) are immensely important due to their ability of recognizing different types of pathogen associated molecular patterns (PAMPs). This study reviews the polymorphic residues present in the nucleotide or in the amino acid sequence of TLRs and their influence on alteration of inflammatory signalling pathways promoting either susceptibility or resistance to major infectious diseases, including tuberculosis, leishmaniasis, malaria and filariasis. Population‐based studies exploring TLR polymorphisms in humans are primarily emphasized to discuss the association of the polymorphic residues with the occurrence and epidemiology of the mentioned infectious diseases. Principal polymorphic residues in TLRs influencing immunity to infection are mostly single nucleotide polymorphisms (SNPs). I602S (TLR1), R677W (TLR2), P554S (TLR3), D299G (TLR4), F616L (TLR5), S249P (TLR6), Q11L (TLR7), M1V (TLR8), G1174A (TLR9) and G1031T (TLR10) are presented as the major influential SNPs in shaping immunity to pathogenic infections. The contribution of these SNPs in the structure‐function relationship of TLRs is yet not clear. Therefore, molecular studies on such polymorphisms can improve our understanding on the genetic basis of the immune response and pave the way for therapeutic intervention in a more feasible way.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31054156</pmid><doi>10.1111/sji.12771</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-7441-6426</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Amino acid sequence Epidemiology Filariasis Genetic factors Immune response Immunosurveillance Infections infectious disease Infectious diseases Inflammation Leishmaniasis Malaria Parasitic diseases pathogen‐associated molecular pattern polymorphism Population studies Residues resistance Signal transduction Single-nucleotide polymorphism Structure-function relationships susceptibility TLR1 protein TLR2 protein TLR3 protein TLR4 protein TLR5 protein TLR7 protein TLR9 protein Toll-like receptors toll‐like receptor Tropical diseases Tuberculosis Vector-borne diseases |
title | Toll‐like receptor polymorphism in host immune response to infectious diseases: A review |
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