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 inScandinavian journal of immunology Vol. 90; no. 1; pp. e12771 - n/a
Main Authors Mukherjee, Suprabhat, Huda, Sahel, Sinha Babu, Santi P.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.07.2019
Subjects
Amino acid sequence
Epidemiology
Filariasis
Genetic factors
Immune response
Immunosurveillance
infectious disease
Infectious diseases
Inflammation
Leishmaniasis
Malaria
pathogen‐associated molecular pattern
polymorphism
Population studies
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
polymorphism
toll-like receptor
susceptibility
infectious disease
pathogen-associated molecular pattern
resistance
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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.
AbstractList 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.
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.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.
Author Sinha Babu, Santi P.
Mukherjee, Suprabhat
Huda, Sahel
Author_xml – sequence: 1
  givenname: Suprabhat
  surname: Mukherjee
  fullname: Mukherjee, Suprabhat
  organization: Kazi Nazrul University
– sequence: 2
  givenname: Sahel
  surname: Huda
  fullname: Huda, Sahel
  organization: Visva‐Bharati University
– sequence: 3
  givenname: Santi P.
  orcidid: 0000-0002-7441-6426
  surname: Sinha Babu
  fullname: Sinha Babu, Santi P.
  email: spsinhababu@gmail.com
  organization: Visva‐Bharati University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31054156$$D View this record in MEDLINE/PubMed
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2019 The Foundation for the Scandinavian Journal of Immunology.
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Issue 1
Keywords polymorphism
toll-like receptor
susceptibility
infectious disease
pathogen-associated molecular pattern
resistance
Language English
License 2019 The Foundation for the Scandinavian Journal of Immunology.
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Snippet Immunopolymorphism is considered as an important aspect behind the resistance or susceptibility of the host to an infectious disease. Over the years,...
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SubjectTerms Amino acid sequence
Epidemiology
Filariasis
Genetic factors
Immune response
Immunosurveillance
infectious disease
Infectious diseases
Inflammation
Leishmaniasis
Malaria
pathogen‐associated molecular pattern
polymorphism
Population studies
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
Title Toll‐like receptor polymorphism in host immune response to infectious diseases: A review
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fsji.12771
https://www.ncbi.nlm.nih.gov/pubmed/31054156
https://www.proquest.com/docview/2243791239
https://www.proquest.com/docview/2229232740
Volume 90
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