Autoimmune hepatitis: A comprehensive review

Liberal, Rodrigo; Grant, Charlotte R.; Mieli‐Vergani, Giorgina; Vergani, Diego

doi:10.1016/j.jaut.2012.11.002

Cited by 185 publications

(143 citation statements)

References 144 publications

Supporting

Mentioning

128

Contrasting

Unclassified

Order By: Relevance

“…Chronic liver disease remains a major public health problem worldwide [1][2][3][4][5] and is complicated by progressive fibrosis and cirrhosis. Chronic liver injury, irrespective of etiology, is typically characterized by inflammation and increased deposition of extracellular matrix (ECM) with a greater proportion of fibrillar collagens.…”

mentioning

confidence: 99%

Versican: a novel modulator of hepatic fibrosis

Bukong

Maurice

Chahal

et al. 2016

Laboratory Investigation

View full text Add to dashboard Cite

Little is known about the deposition and turnover of proteoglycans in liver fibrosis, despite their abundance in the extracellular matrix. Versican plays diverse roles in modulating cell behavior in other fibroproliferative diseases, but remains poorly described in the liver. Hepatic fibrosis was induced by carbon tetrachloride treatment of C57BL/6 mice over 4 weeks followed by recovery over a 28-day period. Primary mouse hepatic stellate cells (HSCs) were activated in culture and versican was transiently knocked down in human (LX2) and mouse HSCs. Expression of versican, A Disintegrinlike and Metalloproteinase with Thrombospondin-1 motifs (ADAMTS)-1, -4, -5, -8, -9, -15, and -20, and markers of fibrogenesis were studied using immunohistochemistry, real-time quantitative PCR, and western blotting. Immunohistochemistry showed increased expression of versican in cirrhotic human livers and the mouse model of fibrosis. Carbon tetrachloride treatment led to significant increases in versican expression and the proteoglycanases ADAMTS-5, -9, -15, and -20, alongside TNF-α, α-smooth muscle actin (α-SMA), collagen-1, and TGF-β expression. During recovery, expression of many of these genes returned to control levels. However, expression of ADAMTS-5, -8, -9, and -15 showed delayed increases in expression at 28 days of recovery, which corresponded with decreases in versican V0 and V1 cleavage products (G1-DPEAAE 1401 and G1-DPEAAE 441 ). Activation of primary HSCs in vitro significantly increased versican, α-SMA, and collagen-1 expression. Transient knockdown of versican in HSCs led to decreases in markers of fibrogenesis and reduced cell proliferation, without inducing apoptosis. Versican expression increases during HSC activation and liver fibrosis, and proteolytic processing occurs during the resolution of fibrosis. Knockdown studies in vitro suggest a possible role of versican in modulating hepatic fibrogenesis.

show abstract

mentioning

confidence: 99%

Versican: a novel modulator of hepatic fibrosis

Bukong

Maurice

Chahal

et al. 2016

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…The HLA-DRB1 locus, specially the alleles HLA-DR3 (DRB1*0301) and DR4 (DRB1*0401) are related to AIH type 1 susceptibility in European populations and North Americans and the strongest genetic associations contributing to the diagnosis of AIH and are included in the IAIHG revised diagnostic scoring system [15] . Genetic profile determines the response to treatment: those who do not respond to corticosteroid treatment have usually DRB1*0301 alleles [15] . Also, clinical manifestations and prognosis may be determined by genetic profile.…”

Section: Minireviewsmentioning

confidence: 99%

“…Immunosuppressive treatments should be established immediately, especially in the presence of severe disease [24] . The goal of AIH treatment includes: induction of remission; maintenance of remission; prevention of the establishment of cirrhosis and complications using the lowest possible dose of medication [11,15] . AIH has a good response to immunosuppressive treatment with 80% of remission rate [15,26] .…”

Section: Pharmacologic Treatment Of Aihmentioning

confidence: 99%

Management of autoimmune hepatitis: Focus on pharmacologic treatments beyond corticosteroids

Moura

Liberal

Cardoso

et al. 2014

WJH

View full text Add to dashboard Cite

Core tip: With our review we pretend to describe the non-standard pharmacologic treatments available for autoimmune hepatitis, the indications for its use and the main applications. Also, we pretend to enhance that those alternatives are only available guided by the experience in liver transplant patients and should be only used by experienced centers. The difficult-totreat patients lead to the application of those therapies mainly as salvage treatments.Casal Moura M, Liberal R, Cardoso H, Horta e Vale AM, Macedo G. Management of autoimmune hepatitis: Focus on pharmacologic treatments beyond corticosteroids.

show abstract

“…Se considera que son capaces de promover la respuesta autoinmune por intermedio de los siguientes mecanismos: activación inespecífica de células T en reposo, modificación o liberación de proteínas secuestradas, reacción cruzada entre un virus y una proteína propia del paciente (mecanismo de semejanza molecular) y modulación de la expresión genética. 1,[11][12][13][14] …”

Section: Genética Y Patogeniaunclassified

Hepatitis autoinmune en niños. Perspectivas actuales

2014

View full text Add to dashboard Cite

Hepatitis autoinmune en niños. Perspectivas actualesAutoimmune hepatitis in children. Current perspectives RESUMEN La hepatitis autoinmune es una enfermedad inflamatoria crónica progresiva del hígado de etiología desconocida. Afecta predominantemente al sexo femenino en la etapa prepuberal. Se caracteriza por presentar niveles elevados de transaminasas e inmunoglobulina G, niveles bajos del factor 4a del complemento y de IgA circulantes, autoanticuerpos en suero, prevalencia del antígeno leucocitario humano B8, haplotipos DR3 y DR4, y hepatitis de interfase en la histología. El curso puede ser fluctuante, con períodos de remisión espontánea. Se describen dos tipos de acuerdo con los autoanticuerpos hallados en suero. El mecanismo de producción del daño hepático es secundario a reacciones inmunes contra antígenos hepáticos no controladas adecuadamente por las células T reguladoras. La mayoría de los pacientes responden favorablemente al tratamiento inmunosupresor. Librada a su evolución espontánea, la enfermedad progresa hacia la destrucción hepática, por lo que, en su etapa terminal, requiere un trasplante hepático. Palabras clave: hepatitis autoinmune, niños, diagnóstico, tratamiento.http://dx

show abstract

Autoimmune hepatitis: A comprehensive review

Cited by 185 publications

References 144 publications

Versican: a novel modulator of hepatic fibrosis

Versican: a novel modulator of hepatic fibrosis

Management of autoimmune hepatitis: Focus on pharmacologic treatments beyond corticosteroids

Hepatitis autoinmune en niños. Perspectivas actuales

Contact Info

Product

Resources

About