Polymorphism in the 3′ UTR of the IL12B gene is associated with Chagas’ disease cardiomyopathy

Zafra, German; Morillo, Carlos A.; Martı́n, Javier; González, A. Gustavo; González, Clara Isabel

doi:10.1016/j.micinf.2007.04.010

Cited by 48 publications

(36 citation statements)

References 28 publications

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“…15 Genetic susceptibility to T cruzi has also been studied in different regions and by several investigators. 21,22 Recent studies indicate that the interferon-γ +874T/A genetic polymorphism may be involved in the susceptibility to but not in the progression of Chagas cardiomyopathy, linking inflammatory regulatory genes to the susceptibility to T cruzi infection. 17,18 Finally, autoantibodies directed to β 1 -and β 2 -adrenoreceptors and muscarinic-2 receptors have been documented in asymptomatic carriers and have been used to predict progression to cardiomyopathy, but larger studies are needed to validate these markers.…”

Section: March 12 2013mentioning

confidence: 99%

Infection With Trypanosoma cruzi and Progression to Cardiomyopathy

Morillo

2013

Circulation

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Section: March 12 2013mentioning

confidence: 99%

Infection With Trypanosoma cruzi and Progression to Cardiomyopathy

Morillo

2013

Circulation

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“…However, genetic susceptibility to T. cruzi infection and the development of cardiomyopathy is complex and heterogeneous and likely involves several genes, each with a modest contribution on the pathogenesis of the disease. In fact, genetic studies in human beings have addressed the relation between cytokine and chemokine gene polymorphisms and development of chagasic heart disease [16][17][18][19][20][21][22]. In this study, we investigated the possible association of CCL5/RANTES and CXCL8/interleukin 8 (IL-8) chemokines, and CCR2 and CCR5 chemokines receptors cluster gene polymorphisms with the development of chagasic cardiomyopathy in a case-control study in Colombia endemic area.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants in the chemokines and chemokine receptors in Chagas disease

Flórez¹,

Martín²,

González³

2012

Human Immunology

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“…In addition, the C3F allele has been proposed as a marker for the progression of cardiomyopathy (Messias-Reason et al 2003). Cytokine and chemokine genes have been implicated in determining increased susceptibility and further development of chagasic heart disease (Calzada et al 2001, Flórez et al 2006, Zafra et al 2007). Genetic susceptibility to T. cruzi infection and the development of cardiomyopathy is complex and heterogeneous and likely involves several genes.…”

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confidence: 99%

Polymorphisms of toll-like receptor 2 and 4 genes in Chagas disease

Zafra

Flórez

Morillo

et al. 2008

Mem. Inst. Oswaldo Cruz

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Chagas' disease (CD) is caused by infection with the intracellular protozoan parasite, Trypanosoma cruzi, and is the major cause of cardiomyopathy and heart failure in endemic regions of Colombia and South America (Guhl 1999, WHO 2002. A wide clinical spectrum is observed in the chronic phase of CD, varying from a relatively benign indeterminate form to gastrointestinal compromise or chronic cardiomyopathy that is usually fatal. The fact that only 20-30% of the infected individuals develop cardiomyopathy suggests a differential set of physiopathologic events between infected individuals. Differences in the expression of genes related to the immune response may be involved. In humans there are studies addressing the relation between the major histocompatibility complex genes and CD (Nieto et al. 2000). In addition, the C3F allele has been proposed as a marker for the progression of cardiomyopathy (Messias-Reason et al. 2003). Cytokine and chemokine genes have been implicated in determining increased susceptibility and further development of chagasic heart disease (Calzada et al. 2001, Flórez et al. 2006, Zafra et al. 2007). Genetic susceptibility to T. cruzi infection and the development of cardiomyopathy is complex and heterogeneous and likely involves several genes. The toll-like receptor family (TLRs) is a major class of eukaryotic receptors for microbial pathogens associated molecular patterns (PAMPs) and endogenous ligands. When TLRs recognize PAMPs induce signals responsible for the activation of genes relevant to the host defence including inflammatory and adaptative immunerelated cytokines (Takeda et al. 2003). Some of the microbial components recognized by these receptors have been identified. TLR2 recognizes a variety of microbial components such as lipoproteins from various pathogens, and lipoarabinomannan from mycobacteria and zymosan from fungi, among others. TLR4 recognizes principally lipopolysaccharide from Gram-negative bacteria (Takeda & Akira 2005). In protozoa, Plasmodium falciparum glycosylphosphatidylinositol (GPI) was reported to induce signaling via both TLR-2 and TLR-4 (Krishnegowda et al. 2005). GPI anchors of T. cruzi are recognized by TLR2 ). In addition T. cruzi Tc52 released protein and glycoinositolphospholipid, stimulating murine macrophages via TLR2 and TLR4 (Ouassi et al. 2002, Oliveira et al. 2004. Unmethylated CpG motifs of T. cruzi DNA also stimulate macrophages, dendritic cells and B lymphocytes probably via TLR-9 (Shoda et al. 2001). Some reports have shown that TLR-2, TLR-4 and the related signalling pathway play an important role in the initial recognition of T. cruzi and may regulate the initial pro-inflammatory response during infection with the parasite but may also contribute to the severity of the disease (Almeida & Gazzinelli 2001).Genetic variations in TLR genes correlate with several infectious diseases (Schroder et al. 2005). Several single-nucleotide polymorphism (SNPs) have been described for the TLR2 and TLR4 genes. The TLR2 argin- 28 ine to glutamine subst...

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Polymorphism in the 3′ UTR of the IL12B gene is associated with Chagas’ disease cardiomyopathy

Cited by 48 publications

References 28 publications

Infection With Trypanosoma cruzi and Progression to Cardiomyopathy

Infection With Trypanosoma cruzi and Progression to Cardiomyopathy

Genetic variants in the chemokines and chemokine receptors in Chagas disease

Polymorphisms of toll-like receptor 2 and 4 genes in Chagas disease

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