TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children

Berdelı, Afig; Celik, Handan; Özyürek, Ruhi; Dogrusoz, Buket; Aydin, Hikmet Hakan

doi:10.1007/s00109-005-0677-x

Cited by 118 publications

(81 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data are supported by previous reports of populations from Germany (39,47,59), Turkey (6,14), Iran (1), and the Netherlands (58). A clear difference, however, was present in the Vlax-Roma, gypsies living in Bosnia-Herzegovina, Romania, Albania, and Hungary (30), in which a small number of individuals were heterozygous for this polymorphism.…”

Section: Discussionsupporting

confidence: 92%

Different Patterns of Toll-Like Receptor 2 Polymorphisms in Populations of Various Ethnic and Geographic Origins

et al. 2012

View full text Add to dashboard Cite

ABSTRACTUpon the invasion of the host by microorganisms, innate immunity is triggered through pathogen recognition by pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are the best-studied class of PRRs, and they recognize specific pathogen-associated molecular patterns (PAMPs) from various microorganisms. A large number of studies have shown that genetic variation in TLRs may influence susceptibility to infections. We assessed the genetic variation ofTLR2, which encodes one of the most important TLRs, in various populations around the globe and correlated it with changes in the function of the molecule. The three best-known nonsynonymousTLR2polymorphisms (1892C>A, 2029C>T, and 2258G>A) were assessed in different populations from the main continental masses: Romanians, Vlax-Roma, Dutch (European populations), Han Chinese (East Asia), Dogon, Fulani (Africa), and Trio Indians (America). The 2029C>T polymorphism was absent in both European and non-European populations, with the exception of the Vlax-Roma, suggesting that this polymorphism most likely arose in Indo-Aryan people after migration into South Asia. The 1892C>A polymorphism that was found exclusively in European populations, but not in Asian, African, or American volunteers, probably occurred in proto-Indo-Europeans. Interestingly, 2258G>A was present only in Europeans, including Vlax-Roma, but at a very low frequency. The differential pattern of theTLR2polymorphisms in various populations may explain some of the differences in susceptibility to infections between these populations.

show abstract

Section: Discussionsupporting

confidence: 92%

Different Patterns of Toll-Like Receptor 2 Polymorphisms in Populations of Various Ethnic and Geographic Origins

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Recent studies suggested that TLR may regulate and contribute to the pathogenesis of diseases with non-infectious tissue injury, since elevated expression of TLRs has been described in such diseases or pathological states [10,53], and TLR polymorphisms have been associated with the susceptibility to certain diseases [54][55][56][57]. For example, inactivation of the MyD88 pathway led to a reduction in atherosclerosis through a decrease in macrophage recruitment to the artery wall that was associated with reduced chemokine levels [58].…”

Section: Tlrs and Lung Injurymentioning

confidence: 99%

The role of Toll-like receptors in non-infectious lung injury

et al. 2006

View full text Add to dashboard Cite

The role of Toll-like receptors (TLRs) in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Previously, we and others have demonstrated that fragmented hyaluronan (HA) accumulates during tissue injury. CD44 is required to clear HA during tissue injury, and impaired clearance of HA results in unremitting inflammation. Additionally, fragmented HA stimulates the expression of inflammatory genes by inflammatory cells at the injury site. Recently, we identified that HA fragments require both TLR2 and TLR4 to stimulate mouse macrophages to produce inflammatory chemokines and cytokines. In a non-infectious lung injury model, mice deficient in both TLR2 and TLR4 show an impaired transepithelial migration of inflammatory cells, increased tissue injury, elevated lung epithelial cell apoptosis, and decreased survival. Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR-dependent basal activation of NF-kB. The exaggerated injury in TLR2 and TLR4 deficient mice appears to be due to impaired HA-TLR interactions on epithelial cells. These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury.

show abstract

“…Immunology of mitral valve stenosis are strongly associated with the pathogenesis of acute RF and may indeed intensify the inflammatory reactions taking place. 22,23 Furthermore, researchers are in the early stages of understanding several other genes associated with enhanced RHD progression. These include polymorphisms of ficolin-2, a pattern-recognition protein important to the lectin complement pathway; 24 C-509T and T869C polymorphisms of transforming growth factor β-1, a cytokine secreted by most immune cells that controls their differentiation, proliferation, and state of function; 25,26 and polymorphism of interleukin 1 (IL-1) receptor antagonist, a cytokine that normally modulates IL-1-related inflammatory processes.…”

Section: Genetic Predispositionmentioning

confidence: 99%

The immunology of mitral valve stenosis

Artola¹,

Mihos²,

Santana³

2011

IJICMR

View full text Add to dashboard Cite

Although the prevalence of rheumatic heart disease (RHD) has rapidly subsided over the last several decades in the United States, it still remains a serious cardiovascular disorder across the world, particularly in developing nations. Chronic autoimmune inflammation of the cardiac valves can result in mitral stenosis, increasing the risk of morbidity, mortality, and long-term sequelae in these patients. Researchers have begun to unravel the mysteries behind the development of RHD in the setting of chronic autoimmune inflammatory reactions and the roles genetic predisposition, antibody-and T-cell-mediated molecular mimicry, and cytokine proinflammatory responses play. In this article, the immunologic pathogenesis of RHD and its effects on the mitral valve are reviewed.

show abstract

TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children

Cited by 118 publications

References 39 publications

Different Patterns of Toll-Like Receptor 2 Polymorphisms in Populations of Various Ethnic and Geographic Origins

Different Patterns of Toll-Like Receptor 2 Polymorphisms in Populations of Various Ethnic and Geographic Origins

The role of Toll-like receptors in non-infectious lung injury

The immunology of mitral valve stenosis

Contact Info

Product

Resources

About