Increased serum immunoglobulin G1 levels in hepatitis C virus infection

Musset, Lucile; Lunel, F; Cacoub, P.; Mannant, P.-R.; Silvain, Christine; Lacombe, Christian; Opolon, P; Preud’homme, Jean-Louis

doi:10.1002/hep.1840210644

Cited by 13 publications

(9 citation statements)

References 12 publications

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“…The multiplex LC-MS-MRM method of Ig subclass quantification has good performance and can be used efficiently for evaluation of immunoglobulin concentrations under any disease context. The results are based on a small set of samples but confirm clearly the reported non-uniform changes in Ig-subclass concentrations in liver disease [6;7]. But the quantification of immunoglobulins is not major aim of our study.…”

Section: Resultssupporting

confidence: 84%

“…Elevation of plasma immunoglobulin concentrations in chronic HCV infection was reported previously [7]. We have used a novel stable isotope dilution LC-MS-MRM method to evaluate which classes of plasma immunoglobulins change in concentration during liver disease progression to HCC.…”

Section: Resultsmentioning

confidence: 90%

“…Correlation analysis indicates a positive correlation between IgG1 and IgG3 with spearman correlation coefficient 0.46 (p<0.01). This might reflect co-regulation of the genes co-localized on chromosome 14 but separated from IgG2 and IgG4 [7]. …”

Section: Discussionmentioning

confidence: 99%

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Quantitative analysis of immunoglobulin subclasses and subclass specific glycosylation by LC–MS–MRM in liver disease

Yuan

Šanda

et al. 2015

Journal of Proteomics

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Aberrant glycosylation of IgGs has been linked to human diseases, including liver disease. In this study, we have quantified plasma immunoglobulins in cirrhosis (CIR) and hepatocellular carcinoma (HCC) and employed a novel LC-MS-MRM assay to quantify glycoforms of IgG subclasses 1-4. Glycan oxonium ions and peptide-GlcNAc fragment ions were utilized to quantify the IgG glycoforms purified by affinity chromatography with normalization to the unique peptide for each IgG subclass. Our results indicate that HCC patients have increased circulating IgG1, IgG3, IgA1, and IgM compared to healthy controls; comparison of HCC and CIR patients shows that HCC patients have significantly higher concentration of IgG1 and IgM but lower concentration of IgG2. Increase in galactose-deficient core fucosylated glycoforms was consistently observed in CIR and HCC patients. The FA2G0 and FA2BG0 glycoforms increase approximately 2-fold in all IgG subclasses accompanied by a decrease in the FA2G2 glycoform. Fucosylation changes are less pronounced but we have detected increased degree of fucosylation in the IgG1 and IgG3 glycoforms. In conclusion, we have optimized a sensitive and selective LC-MS-MRM method for quantification of immunoglobulin subclasses and their site specific glycoforms, demonstrating that both quantities and glycoforms of immunoglobulins change significantly in liver disease progression to HCC.

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Section: Resultssupporting

confidence: 84%

Section: Resultsmentioning

confidence: 90%

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Quantitative analysis of immunoglobulin subclasses and subclass specific glycosylation by LC–MS–MRM in liver disease

Yuan

Šanda

et al. 2015

Journal of Proteomics

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“…The influence of chronic antigen exposure on the B cell compartment is less clear, but hepatitis C-infected individuals demonstrate humoral aberrations that are similar to HIV + individuals: profound hypergammaglobulinemia consisting of non-virus-specific antibodies [33,34] produced by oligoclonally-activated B-cells [35,36] and relatively late emergence of HCV humoral immunity, with antibodies to hepatitis C envelope and core proteins appearing by 6–8 weeks after infection [37–40]. A portion of these antibodies exhibit neutralizing capacity through interference with viral binding to cellular targets such as SRBI, CD81 and claudin-1 [41,42], but the presence of neutralizing antibodies is not clearly associated with early resolution of infection in chimpanzee experiments and human series [39,40,43–55].…”

Section: B Cells and Hcv Infectionmentioning

confidence: 99%

T-bet-expressing B cells during HIV and HCV infections

Knox

Kaplan

Betts

2017

Cellular Immunology

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T-bet-expressing B cells, first identified as perpetuators of autoimmunity, were recently shown to be critical for murine antiviral responses. While their role in human viral infections remains unclear, B cells expressing T-bet or demonstrating a related phenotype have been described in individuals chronically infected with HIV or HCV, suggesting these cells represent a component of human antiviral responses. In this review, we discuss the induction of T-bet in B cells following both HIV and HCV infections, the factors driving T-bet+ B cell expansions, T-bet’s relationship to atypical memory B cells, and the consequences of T-bet induction. We propose potential antiviral roles for T-bet+ B cells and discuss whether this population poses any utility to the HIV and HCV immune responses.

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“…Over 70% of the persistently infected individuals develop chronic hepatic inflammation (hepatitis), which progresses to cirrhosis in approximately 20-30% of infected individuals usually over the course of 2-3 decades [2]. Hepatitis C infection is characterized by profound hyperglobulinemia consisting of nonvirus-specific antibodies [3,4] produced by oligoclonally-activated B-cells [5,6]. Somewhat unexpectedly, chronic B-cell activation in chronic hepatitis C does not result in expansion of the memory B-cell pool in cohorts of mostly non-cirrhotic individuals [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Peripheral CD27−CD21− B-cells represent an exhausted lymphocyte population in hepatitis C cirrhosis

Doi

Tanoue

Kaplan

2014

Clinical Immunology

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Hepatitis C cirrhosis is associated with a profound disappearance of memory B-cells. We sought to determine if this loss is associated with the expansion of the CD27 − CD21 − tissue-like memory B-cells with features of B-cell exhaustion. To this end, we quantified the frequency of CD27 − CD21 − B-cells in healthy, non-cirrhotic HCV-infected, and cirrhotic patients. We examined the expression of putative inhibitory receptors, the proliferative and immunoglobulin-secreting capacity of CD27/CD21-defined B-cell subsets upon B-cell receptor and/or CD40 stimulation. We found that CD27 − CD21 − B-cells are significantly increased in frequency relative to healthy donors in HCV-infected patients. CD27 − CD21 − B-cells were hypoproliferative relative to naïve and resting memory B-cells upon agonistic stimulation, but retained similar capacity for antibody secretion. Conclusion: CD27 − CD21 − tissue-like memory B-cells with exhausted proliferation circulate at increased frequency in cirrhotic and non-cirrhotic HCV-infected patients. This B-cell subset does not appear anergic, exhibiting immunoglobulin-secreting capacity on CD40 agonism indistinguishable from other CD27/CD21-defined B-cell subsets.

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Increased serum immunoglobulin G1 levels in hepatitis C virus infection

Cited by 13 publications

References 12 publications

Quantitative analysis of immunoglobulin subclasses and subclass specific glycosylation by LC–MS–MRM in liver disease

Quantitative analysis of immunoglobulin subclasses and subclass specific glycosylation by LC–MS–MRM in liver disease

T-bet-expressing B cells during HIV and HCV infections

Peripheral CD27−CD21− B-cells represent an exhausted lymphocyte population in hepatitis C cirrhosis

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