Role of mannose‐binding lectin‐2 polymorphism in the development of acute cellular rejection after transplantation for hepatitis <scp>C</scp> virus‐induced liver disease

Eurich, Dennis; Boas-Knoop, Sabine; Yahyazadeh, Ali; Neuhaus, R.; Somasundaram, Rajan; Ruehl, Martin; Puhl, Gero; Neumann, Ulf; Bahra, Marcus

doi:10.1111/j.1399-3062.2012.00747.x

Cited by 10 publications

(5 citation statements)

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“…Establishment of HCV infection is at least partly accomplished by successful escape from complement‐mediated effects, such as virus neutralization and lysis (Amet, Ghabril, Chalasani, & Byrd, ; Kim, Meyer, Di Bisceglie, & Ray, ). The involvement of the lectin pathway in hepatitis C has been demonstrated in different ways, mostly showing an effect of MBL deficiency with response to treatment (Eurich et al., ; Matsushita, Hijikata, & Ohta, ) and disease progression (Alves Pedroso et al., ; Eurich et al., ; Koutsounaki et al., ; Melo et al., ; MohammadHossein, Sara, Mohammad, Rasoul, & Ali, ; Segat et al., ). Possibly due to viral mechanisms of complement attenuation, higher levels of lectin pathway recognition proteins and of complement activation seem to be necessary in controlling HCV infection.…”

Section: Discussionmentioning

confidence: 99%

Effects of MASP2 haplotypes and MASP‐2 levels in hepatitis C‐infected patients

Silva

Catarino

Boldt

et al. 2018

Int J Immunogenetics

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Mannan-binding lectin (MBL) and MBL-associated serine protease 2 (MASP-2) are components of the lectin pathway, which activate the complement system after binding to the HCV structural proteins E1 and E2. We haplotyped 11 MASP2 polymorphisms in 103 HCV patients and 205 controls and measured MASP-2 levels in 67 HCV patients and 77 controls to better understand the role of MASP-2 in hepatitis C susceptibility and disease severity according to viral genotype and fibrosis levels. The haplotype block MASP2*ARDP was associated with protection against HCV infection (OR = 0.49, p = .044) and lower MASP-2 levels in controls (p = .021), while haplotype block AGTDVRC was significantly increased in patients (OR = 7.58, p = .003). MASP-2 levels were lower in patients than in controls (p < .001) and in patients with viral genotype 1 or 4 (poor responders to treatment) than genotype 3 (p = .022) and correlated inversely with the levels of alkaline phosphatase, especially in individuals with fibrosis 3 or 4 (R = -.7, p = .005). MASP2 gene polymorphisms modulate basal gene expression, which may influence the quality of complement response against HCV. MASP-2 levels decrease during chronic disease, independently of MASP2 genotypes, most probably due to consumption and attenuation mechanisms of viral origin and by the reduced liver function, the site of MASP-2 production.

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Section: Discussionmentioning

confidence: 99%

Effects of MASP2 haplotypes and MASP‐2 levels in hepatitis C‐infected patients

Silva

Catarino

Boldt

et al. 2018

Int J Immunogenetics

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“…In this regard, Ficolin-2 and MBL were found to bind HCV envelope glycoproteins E1 and E2, activating complement against HCV-infected hepatocytes (Brown et al, 2010;Liu et al, 2009a,b), and MBL deficiency was repeatedly associated with HCV infection (Koutsounaki et al, 2008;Melo et al, 2009;Segat et al, 2007). Whereas early increased Ficolin-2 levels correlated with a better response to treatment (Hu et al, 2013), MBL deficiency was associated with no treatment response (Alves Pedroso et al, 2008;Eurich et al, 2012). Regarding MASP-2, Tulio et al (2011) investigated 104 South-Brazilian patients with chronic hepatitis C and found an association of homozygotes for the p.371D variant with susceptibility to HCV (OR = 6.33 [95%CI = 1.85-21.7], P = 0.003).…”

Section: Hepatitis C (Hcv)mentioning

confidence: 99%

MBL-associated serine proteases (MASPs) and infectious diseases

Beltrame

Boldt

Catarino

et al. 2015

Molecular Immunology

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The lectin pathway of the complement system has a pivotal role in the defense against infectious organisms. After binding of mannan-binding lectin (MBL), ficolins or collectin 11 to carbohydrates or acetylated residues on pathogen surfaces, dimers of MBL-associated serine proteases 1 and 2 (MASP-1 and MASP-2) activate a proteolytic cascade, which culminates in the formation of the membrane attack complex and pathogen lysis. Alternative splicing of the pre-mRNA encoding MASP-1 results in two other products, MASP-3 and MAp44, which regulate activation of the cascade. A similar mechanism allows the gene encoding MASP-2 to produce the truncated MAp19 protein. Polymorphisms in MASP1 and MASP2 genes are associated with protein serum levels and functional activity. Since the first report of a MASP deficiency in 2003, deficiencies in lectin pathway proteins have been associated with recurrent infections and several polymorphisms were associated with the susceptibility or protection to infectious diseases. In this review, we summarize the findings on the role of MASP polymorphisms and serum levels in bacterial, viral and protozoan infectious diseases.

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“…Earlier, Munster et al [60] postulated a beneficial effect of donor's MBL2 X gene variant (promoter, position −221) on lung transplant outcome (better graft and BOS-free survival). However, carrying the same allele in hepatitis-C virus- (HCV-) positive recipients of liver transplants was a risk factor for acute cellular rejection [61]. …”

Section: Mbl In Injury To Peripheral Organsmentioning

confidence: 99%

Mannan-Binding Lectin in Cardiovascular Disease

Pągowska‐Klimek

Cedzyński

2014

BioMed Research International

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Cardiovascular disease remains the leading cause of mortality and morbidity worldwide so research continues into underlying mechanisms. Since innate immunity and its potent component mannan-binding lectin have been proven to play an important role in the inflammatory response during infection and ischaemia-reperfusion injury, attention has been paid to its role in the development of cardiovascular complications as well. This review provides a general outline of the structure and genetic polymorphism of MBL and its role in inflammation/tissue injury with emphasis on associations with cardiovascular disease. MBL appears to be involved in the pathogenesis of atherosclerosis and, in consequence, coronary artery disease and also inflammation and tissue injury after myocardial infarction and heart transplantation. The relationship between MBL and disease is rather complex and depends on different genetic and environmental factors. That could be why the data obtained from animal and clinical studies are sometimes contradictory proving not for the first time that innate immunity is a “double-edge sword,” sometimes beneficial and, at other times disastrous for the host.

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Role of mannose‐binding lectin‐2 polymorphism in the development of acute cellular rejection after transplantation for hepatitis C virus‐induced liver disease

Abstract: MBL-2 polymorphisms and gender are involved in the development of ACR after LT. CC genotype and gender match may be regarded as risk factors for ACR in HCV-positive graft recipients. Further studies are needed to confirm and verify this observation in non-HCV groups as well.

Cited by 10 publications

References 50 publications

Effects of MASP2 haplotypes and MASP‐2 levels in hepatitis C‐infected patients

Effects of MASP2 haplotypes and MASP‐2 levels in hepatitis C‐infected patients

MBL-associated serine proteases (MASPs) and infectious diseases

Mannan-Binding Lectin in Cardiovascular Disease

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