Anti-endothelial cell auto-antibodies in hepatitis C virus mixed cryoglobulinemia

Cacoub, Patrice; Ghillani, Pascale; Révélen, R; Thibault, Vincent; Cálvez, Vincent; Charlotte, Frédéric; Musset, Lucile; Youinou, Pierre; Piette, Jean‐Charles

doi:10.1016/s0168-8278(99)80337-7

Cited by 60 publications

(28 citation statements)

References 37 publications

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“…11 Concentrations of soluble intercellular adhesion molecule 1 were reported to be higher in HCV patients than control subjects, 12 and Cacoub et al reported a possible association between anti-endothelial cell autoantibodies, which are commonly observed in HCV patients but not in other viral diseases, and vasculitis. 13 By analyzing the Japanese population, Song et al have reported that serum concentrations of CRP were greater in subjects with acute coronary syndrome than in a control group, even after adjusting for other risk factors. 14 Taken together, these data suggest that persistent HCV infection may play a role in vascular injury and the subsequent development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Association Between Hepatitis C Virus Core Protein and Carotid Atherosclerosis.

Ishizaka

Takahashi

et al. 2003

Circ J

112

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Section: Discussionmentioning

confidence: 99%

Association Between Hepatitis C Virus Core Protein and Carotid Atherosclerosis.

Ishizaka

Takahashi

et al. 2003

Circ J

112

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“…[202][203][204] The principal nephritogenic HCV antigen seems to be non-enveloped HCV E2 core protein, which is demonstrable in circulating ICs and in glomerular deposits. [205][206][207] IgG3 antibody bound to HCV E2 can interact with the globular domain of C1q, engage B cells through both B cell receptors and TLR7, and elicit production of monoclonal IgMk antibody to polyclonal anti-HCV IgG (rheumatoid factor). [196][197][198][199]208 These soluble, but cryoprecipitable, aggregates of IgG, IgM, viral proteins/nucleic acids, and C1q constitute the mesangial and subendothelial immune deposits found in glomeruli and cause local inflammation through direct interaction with TLRs 3, 7, and 9 on both infiltrating inflammatory cells and/or resident glomerular cells as well as by inducing more classic pathway C activation.…”

Section: T Cellsmentioning

confidence: 99%

Basic and Translational Concepts of Immune-Mediated Glomerular Diseases

Couser

2012

Journal of the American Society of Nephrology

179

155

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Genetically modified immune responses to infections and self-antigens initiate most forms of GN by generating pathogen-and danger-associated molecular patterns that stimulate Toll-like receptors and complement. These innate immune responses activate circulating monocytes and resident glomerular cells to release inflammatory mediators and initiate adaptive, antigen-specific immune responses that collectively damage glomerular structures. CD4 T cells are needed for B cell-driven antibody production that leads to immune complex formation in glomeruli, complement activation, and injury induced by both circulating inflammatory and resident glomerular effector cells. Th17 cells can also induce glomerular injury directly. In this review, information derived from studies in vitro, well characterized experimental models, and humans summarize and update likely pathogenic mechanisms involved in human diseases presenting as nephritis (postinfectious GN, IgA nephropathy, antiglomerular basement membrane and antineutrophil cytoplasmic antibodymediated crescentic GN, lupus nephritis, type I membranoproliferative GN), and nephrotic syndrome (minimal change/FSGS, membranous nephropathy, and C3 glomerulopathies). Advances in understanding the immunopathogenesis of each of these entities offer many opportunities for future therapeutic interventions.

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“…Rather than being the cause, AECA might be a consequence of an immune response against antigens released from damaged endothelium. Although AECA were found in 41% of patients with hepatitis C virus (HCV) mixed cryoglobulinemia, negative results were reported by another study and definite conclusions cannot be drawn because of differences in the methodologies used [16,17]. However, AECA production, as a consequence of EC damage, does not seem to explain the occurrence of these autoantibodies in all conditions.…”

Section: Introductionmentioning

confidence: 97%