Polyclonal T-Cell Responses to Cytochrome P450IID6 Are Associated With Disease Activity in Autoimmune Hepatitis Type 2

Ma, Yuanfang; Bogdanos, Dimitrios P.; Hussain, Munther J.; Underhill, James A.; Bansal, Sanjay; Longhi, Maria Serena; Cheeseman, Paul; Mieli‐Vergani, Giorgina; Vergani, Diego

doi:10.1053/j.gastro.2005.12.020

Cited by 192 publications

(157 citation statements)

References 46 publications

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“…Taken together, these pioneer studies 1,5 raise the possibility that HCV may trigger AIH through a mechanism of molecular mimicry. This issue [6][7][8][9][10] has been recently revisited by Krawitt in New England Journal of Medicine 11 and Manns and Vogel in HEPATOL-OGY.…”

Section: Autoimmune Hepatitis: Of Host and Pathogenmentioning

confidence: 95%

“…4 In addition, Longhi et al stated that on the basis of their own preliminary experiments, p3 induces the highest percentage of interferon-␥-producing CD8 T cells in CYP2D6ϩ/HCVϩ patients. In a previous work of the same group published in Gastroenterology, 5 the investigation of cellular immunity directed against CYP2D6 in AIH showed that apart from AIH patients, patients with HCV infection presented CYP2D6-specific CD4 responses (among 73 pathological controls with various diseases, these responses were found exclusively in HCV-infected patients as 3/6 anti-CYP2D6 antibody-negative HCV patients had significant CD4 responses to a CYP2D6 peptide mimicking HCV).…”

Section: Autoimmune Hepatitis: Of Host and Pathogenmentioning

confidence: 97%

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Autoimmune hepatitis: Of host and pathogen

Rigopoulou

Dalekos

2008

Hepatology

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Section: Autoimmune Hepatitis: Of Host and Pathogenmentioning

confidence: 95%

Section: Autoimmune Hepatitis: Of Host and Pathogenmentioning

confidence: 97%

Autoimmune hepatitis: Of host and pathogen

Rigopoulou

Dalekos

2008

Hepatology

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“…The point of interest heuristically on the serological distinction is that the respective autoantibody responses (ANA/SMA, anti-LKM-1) cannot be ascribed simply to (hepato) cellular injury, an explanation often levelled for the appearance of at least for some types of autoantibody. Although cases of anti-LKM-1-positive AIH are numerically far less than the traditional type, the ratios being about 1:10 in adults and 1:4 in children, type 2 AIH has proven far more amenable to investigation, since the LKM-1 antigen has been molecularly identified by screening a gene expression library as the cytochrome P450 isoform 2D6, enabling epitopes to be mapped [68] ; there is demonstrated a CD4+ T-cell responsiveness to peptide antigens of CYP450 2D6 [69] ; and an experimentally credible model in mice has been developed [70] . Soluble liver/pancreas antigen A soluble cytoplasmic antigen was independently discovered by CF [71] , and ELISA [72] , using pancreas or liver cell extracts respectively, and the reactant was found to be identical; it is generally known as "soluble liver/ pancreas antigen (SLA).…”

Section: Lkm-1 Antigenmentioning

confidence: 99%

Historical reflections on autoimmune hepatitis

Mackay

2008

WJG

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Autoimmune hepatitis (AIH), initially known as chronic active or active chronic hepatitis (and by various other names), first came under clinical notice in the late 1940s. However, quite likely, chronic active hepatitis (CAH) had been observed prior to this and was attributed to a persistently destructive virus infection of the liver. An earlier (and controversial) designation in 1956 as lupoid hepatitis was derived from associated L.E. cell test positivity and emphasized accompanying multisystem features and immunological aberrations. Yo u n g w o m e n f e a t u r e d p r o m i n e n t l y i n e a r l y descriptions of CAH. AIH was first applied in 1965 as a descriptive term. Disease-characteristic autoantibodies were defined from the early 1960s, notably antinuclear antibody (ANA), smooth muscle antibody (SMA) and liver-kidney microsomal (LKM) antibody. These are still widely used diagnostically but their relationship to pathogenesis is still not evident. A liver and disease specific autoantigen has long been searched for but unsuccessfully. Prolonged immunosuppressive therapy with prednisolone and azathioprine in the 1960s proved beneficial and remains standard therapy today. AIH like many other autoimmune diseases is associated with particular HLA alleles especially with the "ancestral" B8, DR3 haplotype, and also with DR4. Looking forwards, AIH is one of the several enigmatic autoimmune diseases that, despite being (relatively) organ specific, are marked by autoimmune reactivities with non-organ-specific autoantigens. New paradigms are needed to explain the occurrence, expressions and pathogenesis of such diseases.

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“…It is characterised by the presence of various autoantibodies in the serum, high level of gammaglobulin and mononuclear cell infiltration in the periportal or portal area histopathologically (motheaten necrosis) (1)(2)(3)(4)(5). According to immunoserologic findings four types of AIH were defined as type 1, type 2, type 3 and undefined autoimmune hepatitis (6)(7)(8)(9)(10)(11). Autoimmune hepatitis occurs mostly at the ages of 10-20 years.…”

Section: Introductionmentioning

confidence: 99%

Otoimmün hepatitli olgularımızın irdelenmesi: 11 yıllık deneyimimiz

Gulec¹,

Urgancı²,

Demirel³

et al. 2012

tpa

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Aim:This study aimed to review a series of patients with autoimmune hepatitis in terms of disease pattern, laboratory results, treatment outcomes and adverse effects of treatment. Material and Method: Children with autoimmune hepatitis were retrospectively reviewed. In all patients, viral and metobolic etiologies were excluded. Patients were classified as type-1, type-2 and non-classified type, as well as acute and chronic groups. Treatment response and cessation of treatment were evaluated. Results: Patients were beetween 4 and 17 years old (12±2.68 years). Twenty patients were female, 11 patients were male. Seventeen percent of the patients were in the acute group and 14% were in the chronic group; 18% were in the type-1 group, 6% were in the type-2 group and 7% were in the non-classified type group. Deflazacort was started in all patients. Azothiopurine (2 mg/kg/day) was added in 10 patients with late response at the end of the third month. Deflazacort dosage was decreased at 6-8 weeks intervals and continued at a maintenance dosage of 5 mg/day. After a two-year period complete response was obtained in 24 patients and partial response was obtained in 5 patients. No response was obtained in 2 patients. During the nine-year follow-up period, treatment was ended in 6 patients. In one patient, there was a recurrance in 6 months; the remaining 5 patients are still being followed up without a problem. Despite treatment, portal hypertension was observed in 5 patients. Conclusions: Early diagnosis and treatment of childhood autoimmune hepatitis can decrease the risk of progression to cirrhosis and can increase the survival. Deflazocort can be a choice instead of prednisolone because of its efficiency in treatment and lesser side effects. (Turk Arch Ped 2012; 47: 29-34)

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Polyclonal T-Cell Responses to Cytochrome P450IID6 Are Associated With Disease Activity in Autoimmune Hepatitis Type 2

Cited by 192 publications

References 46 publications

Autoimmune hepatitis: Of host and pathogen

Autoimmune hepatitis: Of host and pathogen

Historical reflections on autoimmune hepatitis

Otoimmün hepatitli olgularımızın irdelenmesi: 11 yıllık deneyimimiz

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