HLA haplotypes are associated with differential susceptibility to <i>Trypanosoma cruzi</i> infection

Nieto, Antonio; Beraún, Y.; Collado, María; Caballero, Abelardo; Alonso, Álvaro; González, A. Gustavo; Martı́n, Javier

doi:10.1034/j.1399-0039.2000.550301.x

Cited by 50 publications

(32 citation statements)

References 18 publications

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“…Another study on this population in an endemic region revealed an association of the HLA-DRB1*01-DQB1*0501 haplotype with cardiomyopathy [71]. The HLA-DRB1*01-DQB1*0501-DPB1*0401 haplotype is mentioned by Fernández-Mestre et al (2002) as a marker of susceptibility to Chagas' disease in Venezuela [72], while HLA-DRB1*14-DQB1*0301 was associated with noninfection by T. cruzi in individuals inhabiting a highly endemic area in Peru [73]. Overtvelt et al (2002) demonstrated that HLA class I also participates in the escape mechanism of T. cruzi from the immune response, associating greater expression of some of these molecules with longer persistence of the parasite in the host organism without eliciting an immune response [74].…”

Section: Parasitic Infectionsmentioning

confidence: 91%

Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

Alves¹,

Souza²,

Meyer³

et al. 2006

Braz J Infect Dis

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Many studies have tried to identify genetic markers for infectious diseases, some of them have focused on human leukocyte antigens (HLA). The products of HLA genes interact with surfacespecific receptors of T lymphocytes, resulting in activation of the host's immune response. Association of bacterial, viral, parasitic and fungal infections with the host's HLA has been widely investigated. The type and strength of this association differs among distinct populations, as well as among racial and/or ethnic groups. The new molecular methods for the identification of the HLA alleles, and the resulting new nomenclature, have contributed to a better understanding of this system. Unfortunately, this information has not been adequately transmitted to clinicians, which hampers the understanding of the association between the HLA system and diseases. We revised relevant studies on the association of HLA genes with infectious diseases, demonstrating their importance in the pathogenic mechanisms, through increased susceptibility or protection against infections and their complications.

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Section: Parasitic Infectionsmentioning

confidence: 91%

Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

Alves¹,

Souza²,

Meyer³

et al. 2006

Braz J Infect Dis

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“…These two antigens are the most frequent reported in several healthy American populations, including the Mexicans (both Mestizos and Amerindians) [19 -21]. A study in a rural mestizo population from Peru reported a protective effect of the HLA-DR14 DQB1*0301 haplotype in the T. cruzi infection; however, they did not detect association with chagasic heart disease [14]. Other reports suggest associations of cardiac damage with both class I and class II alleles, but the results have been heterogeneous [13].…”

Section: Mhc Class I (Hla-a and -B) And Class Ii (Hla-dr)mentioning

confidence: 99%

“…Murine models revealed that cytotoxic lymphocytes CD8 ϩ T cells are essential to eliminate parasites, and autoimmune mechanisms have been reported to play an important role in the development of chronic Chagas heart disease, both in experimental models and in humans [10,11]. Previous studies have suggested participation of major histocompatibility complex (MHC) genes on the susceptibility or resistance to T. cruzi infection and on the development of cardiac disease [12][13][14][15][16]. Thus, the aim of the present study was to investigate the possible role of MHC genes in determining the susceptibility to Trypanosoma cruzi infection as well as in the development of chagasic heart disease in the Mexican mestizo population.…”

Section: Introductionmentioning

confidence: 99%

MHC class I and class II genes in mexican patients with Chagas disease

Cruz-Robles¹,

Reyes²,

Monteón-Padilla

et al. 2004

Human Immunology

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“…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).…”

mentioning

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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HLA haplotypes are associated with differential susceptibility to Trypanosoma cruzi infection

Cited by 50 publications

References 18 publications

Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

Immunogenetics and infectious diseases: special reference to the mayor histocompatibility complex

MHC class I and class II genes in mexican patients with Chagas disease

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

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