Premium
Association of genetic variants of membrane receptors related to recognition and induction of immune response with H elicobacter pylori infection in E cuadorian individuals
Author(s) -
CabreraAndrade A.,
LópezCortés A.,
Muñoz M. J.,
JaramilloKoupermann G.,
Rodriguez O.,
Leone P. E.,
PazyMiño C.
Publication year - 2014
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12118
Subject(s) - tlr2 , immune system , immunology , biology , pattern recognition receptor , genotype , receptor , innate immune system , pathogen associated molecular pattern , allele , gene , genetics
Summary Helicobacter pylori ( Hp ) has a worldwide distribution showing its higher prevalence of infection in developing countries. Toll‐like receptors (TLRs) and C‐type lectin receptors (CLRs) are proteins that recognize pathogen‐associated molecular patterns (PAMPs) and initiate an innate immune response by promoting growth and differentiation of specialized hematopoietic cells for host defense. Gastric infections led by Hp induce a Th‐1 cellular immune response, regulated mainly by the expression of IFN‐γ. In this retrospective case‐control study, we evaluated the TLR1 1805T/G, TLR2 2029C/T, TLR4 896A/G, CD209 ‐336A/G and IFNGR1 ‐56C/T polymorphisms and their relationship with susceptibility to Hp infection. TLR1 1805T/G showed statistical differences when the control ( Hp ‐) and infected ( Hp +) groups ( P = 0.041*) were compared; the TLR1 1805G allele had a protective effect towards infection (OR = 0.1; 95% CI = 0.01‐0.88, P = 0.033*). Similarly, the IFNGR1 ‐56C/T polymorphism showed statistical differences between Hp + and Hp – ( P = 0.018*), and the IFNGR1 ‐56TT genotype exhibited significant risk to Hp infection (OR = 2.9, 95% CI = 1.27‐6.54, P = 0.018*). In conclusion, the pro‐inflammatory TLR1 1805T and IFNGR1 ‐56T alleles are related with susceptibility to Hp infection in Ecuadorian individuals. The presence of these polymorphisms in individuals with chronic infection increases the risk of cellular damage and diminishes the cellular immune response efficiency towards colonizing agents.