Autoantibodies in Autoimmune Hepatitis

Muratori, Luigi; Deleonardi, Gaia; Lalanne, Claudine; Barbato, Erica; Tovoli, Alessandra; Libra, Alessia; Lenzi, Marco; Cassani, F.; Muratori, Paolo

doi:10.1159/000440748

Cited by 12 publications

(8 citation statements)

References 50 publications

(50 reference statements)

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“…Exposure to respirable cSiO 2 has also been aetiologically linked to several autoimmune diseases besides lupus [66][67][68][69][70][71][72][73]. Thus, it was noteworthy that cSiO 2 induced AAbs associated with rheumatoid arthritis (collagen II, fibrinogen IV, fibrinogen S, fibronectin, and vimentin), Sj€ ogren's syndrome (a-fodrin), systemic sclerosis (topoisomerase I), vasculitis (MPO and PR3), myositis (Mi-2, TIF1-c, MDA5), autoimmune hepatitis (LC-1), and coeliac disease (TTG) [74][75][76][77][78]. Altogether, it might be speculated that these AAgs arise in the lung following chronic exposure to cSiO 2, and subsequently drive the production of AAbs that play pathogenic roles in lupus and these other autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Omega-3 fatty acid intake suppresses induction of diverse autoantibody repertoire by crystalline silica in lupus-prone mice

Rajasinghe

Zhu

et al. 2020

Autoimmunity

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Inhalation of crystalline silica (cSiO 2) in the workplace is etiologically linked to lupus and other autoimmune diseases. Exposing lupus-prone NZBWF1 mice to respirable cSiO 2 unleashes a vicious cycle of inflammation and cell death in the lung that triggers interferon-regulated gene expression, ectopic lymphoid structure (ELS) development, elevation of local and systemic autoantibodies (AAbs), and glomerulonephritis. However, cSiO 2-induced inflammation and onset of autoimmunity can be prevented by inclusion of the x-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) into the diet of these mice. Since cSiO 2 both causes cell death and interferes with efferocytosis, secondary necrosis of residual cell corpses might provide a rich and varied autoantigen (AAg) source in the lung. While it is known that the particle induces anti-nuclear and anti-dsDNA AAbs in NZBWF1 mice, the full extent of the cSiO 2-induced AAb response relative to specificity and isotype is not yet understood. The purpose of this study was to test the hypotheses that cSiO 2 exposure induces a wide spectrum of AAbs in the pulmonary and systemic compartments, and that dietary DHA intervention prevents these changes. Archived tissue fluid samples were obtained from a prior study in which NZBWF1 mice were fed purified isocaloric diets containing no DHA (control) or DHA corresponding calorically to human doses of 2 and 5 g/day. Mice were intranasally instilled with 1 mg cSiO 2 or saline vehicle weekly for 4 weeks, then groups euthanized 1, 5, 9, or 13 weeks post-instillation (PI) of the last cSiO 2 dose. Bronchoalveolar lavage fluid (BALF) and plasma from each time point were subjected to AAb profiling using a microarray containing 122 AAgs. cSiO 2 triggered robust IgG and IgM AAb responses against lupus-associated AAgs, including DNA, histones, ribonucleoprotein, Smith antigen, Ro/SSA, La/SSB, and complement as early as 1 week PI in BALF and 5 weeks PI in plasma, peaking at 9 and 13 weeks PI, respectively. Importantly, cSiO 2 also induced AAbs to AAgs associated with rheumatoid arthritis (collagen II, fibrinogen IV, fibrinogen S, fibronectin, and vimentin), Sj€ ogren's syndrome (a-fodrin), systemic sclerosis (topoisomerase I), vasculitis (MPO and PR3), myositis (Mi-2, TIF1-c, MDA5), autoimmune hepatitis (LC-1), and celiac disease (TTG). cSiO 2 elicited comparable but more modest IgA AAb responses in BALF and plasma. cSiO 2-induced AAb production was strongly associated with time dependent inflammatory/autoimmune gene expression, ELS development, and glomerulonephritis. AAb responses were dose-dependently suppressed by DHA supplementation and negatively correlated with the x-3 index, an erythrocyte biomarker of x-3 content in tissue phospholipids. Taken together, these findings suggest that cSiO 2 exposure elicits a diverse multi-isotype repertoire of AAbs, many of which have been reported in individuals with lupus and other autoimmune diseases. Furthermore, induction of this broad AAb spectrum could be impeded by increasing x-3 tissue content v...

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Section: Discussionmentioning

confidence: 99%

Omega-3 fatty acid intake suppresses induction of diverse autoantibody repertoire by crystalline silica in lupus-prone mice

Rajasinghe

Zhu

et al. 2020

Autoimmunity

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“…ANA has been positively correlated with range of motion of diseases and responds to autoantibodies leading to inflammation and aggravation of the liver tissue damage in patients with AILD (6,7). AMA is an autoantibody without organ specificity and observation of its higher levels signified necrosis, apoptosis or lymphoid infiltration into the intra-hepatic bile ducts (8).…”

Section: Discussionmentioning

confidence: 99%

Evolution of correlation between Helicobacter pylori infection and autoimmune liver disease

Peng

Chen

et al. 2017

Experimental and Therapeutic Medicine

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The present study was planned to evaluate correlation between Helicobacter pylori (HP) infection and autoimmune liver disease (AILD). A total of 60 patients diagnosed with AILD in Affiliated Hospital of Binzhou Medical College were continuously enrolled in the present study. HP infection was detected by 13C-urea breath test. The levels of anti-myeloperoxidase were tested by ELISA. The positive rate of anti-nuclear antibody (ANA), anti-mitochondrial antibody (AMA), anti-smooth muscle antibody (SMA) and anti-neutrophil cytoplasm antibody (ANCA) were tested by indirect immunofluorescence. The positive rates of anti-mitochondrial antibody (AMA-M2), anti-liver-kidney microsomal antibody (LKM-1), anti-liver cytoplasm antibody I (LC-1) and anti-soluble liver antigen/liver-pancreas antigen (SLA/LP) were tested by immunoblotting. Liver function indexes including alanine transaminase, aspartate transaminase, alkaline phosphatase and glutamyltransferase, were analyzed with a fully automatic biochemical analyzer. The levels of serum cytokine IFN-γ, interleukin-6 (IL-6), IL-10 and tumor necrosis factor-α (TNF-α) were tested by ELISA. A total of 37 patients (61.67%) were observed to be HP-positive. MPO-positive rate, positive rate of ANA, AMA, SMA and ANCA and positive rate of AMA-M2, LKM-1, LC-1 and SLA/LP in patients with positive HP infection were significantly higher than those of patients with negative HP infection. On the other hand, the levels of liver function indices did not showed any significant differences among HP-positive cases or HP-negative cases. However, the levels of IFN-γ, IL-6, IL-10 and TNF-α in patients with positive HP infection were significantly higher than those of patients with negative HP infection. In conclusion, the positive infection rate of HP infection in patients with AILD is high and is closely associated with various positive immune antibodies as well as cytokine levels.

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“…Finally, less specific autoantibodies may be detected in a subset of patients, including anticardiolipin, anti-chromatin, anti-dsDNA, rheumatoid factor (RF), anti-histones, anti-Ro/SSA, and anti-cyclic citrullinated peptides (anti-CCP) antibodies. Serum ANA were the first autoantibodies observed in AIH sera over 50 years ago and remain the most sensitive marker of AIH 46 . These most frequently produce a homogeneous or speckled pattern.…”

Section: Autoantibodiesmentioning

confidence: 99%

Rheumatic Manifestations in Autoimmune Liver Disease

Selmi

Generali

Gershwin

2018

Rheumatic Disease Clinics of North America

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Autoimmune liver diseases coexist with rheumatic disorders in approximately 30% of cases and may also share pathogenic mechanisms. Autoimmune liver diseases result from an immune-mediated injury of different tissues, with autoimmune hepatitis (AIH) targeting hepatocytes, and primary biliary cholangitis (PBC) and primary sclerosing cholangitis targeting cholangiocytes. Sjogren syndrome is diagnosed in 7% of AIH cases and serologic autoimmunity profiles are a common laboratory abnormality, particularly in the case of serum antimitochondrial (PBC) or anti-liver kidney microsomal antibodies (AIH). Therapeutic strategies may overlap between rheumatic and autoimmune liver diseases and practitioners should be vigilant in managing bone loss.

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Autoantibodies in Autoimmune Hepatitis

Cited by 12 publications

References 50 publications

Omega-3 fatty acid intake suppresses induction of diverse autoantibody repertoire by crystalline silica in lupus-prone mice

Omega-3 fatty acid intake suppresses induction of diverse autoantibody repertoire by crystalline silica in lupus-prone mice

Evolution of correlation between Helicobacter pylori infection and autoimmune liver disease

Rheumatic Manifestations in Autoimmune Liver Disease

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