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Article: Hepatitis C and D, retroviruses and autoimmune manifestations.

Obermayer-Straub, P / Manns, M P

2001 Volume 16, Issue 3, Page(s) 275–285

Abstract: Chronic infections with hepatitis C virus (HCV) are associated with various autoimmune manifestations, i.e. mixed cryoglobulinemia, membranoproliferative glomerulonephritis, autoimmune thyroid diseases, sporadic porphyria cutanea tarda and B cell ... ...

Abstract	Chronic infections with hepatitis C virus (HCV) are associated with various autoimmune manifestations, i.e. mixed cryoglobulinemia, membranoproliferative glomerulonephritis, autoimmune thyroid diseases, sporadic porphyria cutanea tarda and B cell lymphoma. Since exacerbation of hepatitis occurs in 5-10% of HCV patients receiving interferon-alpha treatment and may be successfully treated by immunosuppression afterwards, hepatitis C was also suspected to be associated with autoimmune hepatitis. LKM3 autoantibodies in chronic hepatitis D virus (HDV) infection and epitope recognition are discussed. Lately, endogenous and exogenous retroviruses have been investigated for the induction of autoimmune diseases. Human A type retroviral particles (HIAP), reverse transcriptase activity and anti-HIAP autoantibodies were detected in patients with Sjögren's syndrome. Anti-HIAP and anti-HIV p24 autoantibodies are seen in systemic lupus erythematosus, primary biliary cirrhosis and multiple sclerosis. Multiple sclerosis was even associated with a new human retrovirus called multiple sclerosis associated retrovirus (MSRV). In diabetes long terminal repeats (LTR) were detected in the HLA DQB1 locus, which was shown to associate with an increased risk of diabetes. A second retrovirus called IDDMK(1,2)22 was reported to code for a superantigen, which was implicated as a potential cause of diabetes. This hypothesis, however, was challenged repeatedly. Until now it is unknown whether endogenous retroviruses are aetiological agents of autoimmune diseases or an epiphenomenon, induced by coinfecting viruses (e.g. herpes viruses) and inflammatory processes.
MeSH term(s)	Autoimmunity/immunology ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/virology ; Hepacivirus/immunology ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/epidemiology ; Hepatitis C, Chronic/immunology ; Hepatitis D, Chronic/immunology ; Hepatitis Delta Virus/immunology ; Humans ; Liver Cirrhosis, Biliary/immunology ; Liver Cirrhosis, Biliary/virology ; Retroviridae/immunology ; Sjogren's Syndrome/immunology ; Sjogren's Syndrome/virology
Language	English
Publishing date	2001-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639452-8
ISSN	0896-8411
ISSN	0896-8411
DOI	10.1006/jaut.2000.0488
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Article: Autoimmunity in liver diseases.

Strassburg, C P / Obermayer-Straub, P / Manns, M P

Clinical reviews in allergy & immunology

2000 Volume 18, Issue 2, Page(s) 127–139

MeSH term(s)	Autoimmune Diseases/immunology ; Autoimmune Diseases/physiopathology ; Autoimmune Diseases/virology ; Autoimmunity/immunology ; Hepatitis D/immunology ; Hepatitis D/physiopathology ; Hepatitis D/virology ; Hepatitis, Viral, Human/immunology ; Hepatitis, Viral, Human/physiopathology ; Hepatitis, Viral, Human/virology ; Humans ; Liver Diseases/immunology ; Liver Diseases/physiopathology ; Polyendocrinopathies, Autoimmune/immunology
Language	English
Publishing date	2000-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1239045-8
ISSN	1559-0267 ; 1080-0549
ISSN (online)	1559-0267
ISSN	1080-0549
DOI	10.1385/CRIAI:18:2:127
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Article: Autoimmune polyglandular syndrome type 1.

Obermayer-Straub, P / Strassburg, C P / Manns, M P

Clinical reviews in allergy & immunology

2000 Volume 18, Issue 2, Page(s) 167–183

MeSH term(s)	Amino Acid Sequence ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Molecular Sequence Data ; Polyendocrinopathies, Autoimmune/complications ; Polyendocrinopathies, Autoimmune/genetics ; Polyendocrinopathies, Autoimmune/physiopathology ; Transcription Factors/chemistry ; Transcription Factors/genetics ; AIRE Protein
Chemical Substances	Transcription Factors
Language	English
Publishing date	2000-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1239045-8
ISSN	1559-0267 ; 1080-0549
ISSN (online)	1559-0267
ISSN	1080-0549
DOI	10.1385/CRIAI:18:2:167
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Article: Autoimmune hepatitis.

Obermayer-Straub, P / Strassburg, C P / Manns, M P

Journal of hepatology

2000 Volume 32, Issue 1 Suppl, Page(s) 181–197

Abstract: Autoimmune hepatitis (AIH) is a rare disease, characterized by female predominance, hypergammaglobulinemia, autoantibodies, association with HLA DR3 and HLA DR4 and a good response to immunosuppression. Different subtypes of AIH may be distinguished, ... ...

Abstract	Autoimmune hepatitis (AIH) is a rare disease, characterized by female predominance, hypergammaglobulinemia, autoantibodies, association with HLA DR3 and HLA DR4 and a good response to immunosuppression. Different subtypes of AIH may be distinguished, based on differences in the autoantibody patterns. AIH type 1 is characterized by anti-nuclear (ANA) and/or anti-smooth muscular (SMA) autoantibodies. AIH type 2 is characterized by liver/kidney microsomal autoantibodies (LKM). AIH type 3 may be distinguished by autoantibodies to soluble liver proteins (SLA) or the liver pancreas antigen (LP). AIH-2 affects predominantly pediatric patients and is characterized by a more severe clinical course, a higher frequency of relapse under immunosuppressive treatment and a more frequent progression to cirrhosis. In contrast, AIH types 1 and 3 show a higher age of onset and a better long-term response to immunosuppressive treatment. At present, the treatment of choice is prednisone alone or a combination with prednisone and azathioprine. Both treatment protocols show high survival rates. However, a rate of 13% of treatment failures and the failure to induce permanent remission in most patients underlines the urgent need to develop additional treatment regimens. A yet unknown genetic predisposition is believed to act as the underlying etiological factor in AIH. This genetic predisposition includes a few known risk factors such as the presence of HLA DR3 or HLA DR4, deletions of C4A alleles and female gender. Furthermore, it has to be postulated that defects in immunoregulatory genes exist. A model for such defects may be the autoimmune polyglandular syndrome type 1 (APS1), which results from the defects in a single gene, the autoimmune regulator type 1 (AIRE-1). Patients with APS1 suffer from mucocutaneous candidiasis and a number of organ-specific autoimmune diseases. Characteristic is a high variability in the number and character of the disease components in APS1, indicating that other genetic and environmental factors may strongly modulate the outcome of disease. Environmental factors may comprise chemical influences, such as nutritional compounds and drugs, or virus infections. Several drugs or chemicals were shown to induce hepatitis with autoimmune involvement, e.g. tienilic acid, dihydralazine and halothane. Adduct formation of an activated metabolite is believed to act as a trigger and to induce a specific immune response. Similarly, viruses were repeatedly shown to trigger autoimmune hepatitis. In virus infections, sequence similarities between viral and self-proteins may trigger autoimmune processes and the simultaneous presence of inflammatory cytokines during virus infection may further increase the risk of developing self-perpetuating autoimmune reactions which overshoot.
MeSH term(s)	Autoantibodies/analysis ; Genetic Predisposition to Disease ; Hepatitis, Autoimmune/complications ; Hepatitis, Autoimmune/genetics ; Hepatitis, Autoimmune/immunology ; Hepatitis, Autoimmune/therapy ; Humans ; Polyendocrinopathies, Autoimmune/complications ; Prognosis
Chemical Substances	Autoantibodies
Language	English
Publishing date	2000
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/s0168-8278(00)80425-0
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Article: Target proteins in human autoimmunity: cytochromes P450 and UDP- glucuronosyltransferases.

Obermayer-Straub, P / Strassburg, C P / Manns, M P

Canadian journal of gastroenterology = Journal canadien de gastroenterologie

1999 Volume 14, Issue 5, Page(s) 429–439

Abstract: Cytochromes P450 (CYPs) and UDP-glucuronosyltransferases (UGTs) are targets of autoantibodies in several hepatic and extrahepatic autoimmune diseases. Autoantibodies directed against hepatic CYPs and UGTs were first detected by indirect ... ...

Abstract	Cytochromes P450 (CYPs) and UDP-glucuronosyltransferases (UGTs) are targets of autoantibodies in several hepatic and extrahepatic autoimmune diseases. Autoantibodies directed against hepatic CYPs and UGTs were first detected by indirect immunofluorescence as antiliver and/or kidney microsomal antibodies. In autoimmune hepatitis (AIH) type 2, liver and/or kidney microsomal (LKM) type 1 autoantibodies are detected and are directed against CYP2D6. About 10% of AIH-2 sera further contain LKM-3 autoantibodies directed against family 1 UGTs. Chronic infections by hepatitis C virus and hepatitis delta virus may induce several autoimmune phenomena, and multiple autoantibodies are detected. Anti-CYP2D6 autoantibodies are detected in up to 4% of patients with chronic hepatitis C, and anti-CYP2A6 autoantibodies are detected in about 2% of these patients. In contrast, 14% of patients with chronic hepatitis delta virus infections generate anti-UGT autoantibodies. In a small minority of patients, certain drugs are known to induce immune-mediated, idiosyncratic drug reactions, also known as 'druginduced hepatitis'. Drug-induced hepatitis is often associated with autoantibodies directed against hepatic CYPs or other hepatic proteins. Typical examples are tienilic acid-induced hepatitis with anti-CYP2C9, dihydralazine hepatitis with anti-CYP1A2, halothane hepatitis with anti-CYP2E1 and anticonvulsant hepatitis with anti-CYP3A. Recent data suggest that alcoholic liver disease may be induced by mechanisms similar to those that are active in drug-induced hepatitis. Autoantibodies directed against several CYPs are further detected in sera from patients with the autoimmune polyglandular syndrome type 1. Patients with autoimmune polyglandular syndrome type 1 with hepatitis often develop anti-CYP1A2; patients with adrenal failure develop anti-CYP21, anti- CYP11A1 or CYP17; and patients with gonadal failure develop anti-CYP11A1 or CYP17. In idiopathic Addison disease, CYP21 is the major autoantigen.
MeSH term(s)	Autoantibodies/physiology ; Autoimmunity ; Chemical and Drug Induced Liver Injury/immunology ; Cytochrome P-450 CYP2D6/immunology ; Cytochrome P-450 CYP2E1/immunology ; Cytochrome P-450 Enzyme System/immunology ; Dihydralazine/adverse effects ; Glucuronosyltransferase/immunology ; Hepatitis C, Chronic/immunology ; Hepatitis, Autoimmune/immunology ; Humans ; Polyendocrinopathies, Autoimmune/immunology
Chemical Substances	Autoantibodies ; Cytochrome P-450 Enzyme System (9035-51-2) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-) ; Cytochrome P-450 CYP2D6 (EC 1.14.14.1) ; Glucuronosyltransferase (EC 2.4.1.17) ; Dihydralazine (PCU411F5L6)
Language	English
Publishing date	1999-04-19
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639439-5
ISSN	1916-7237 ; 0835-7900
ISSN (online)	1916-7237
ISSN	0835-7900
DOI	10.1155/2000/910107
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Article: Autoimmune polyglandular syndromes.

Obermayer-Straub, P / Manns, M P

Bailliere's clinical gastroenterology

1998 Volume 12, Issue 2, Page(s) 293–315

Abstract: Autoimmune polyglandular syndrome type 1 (APS1) is characterized by a variable combination of disease components: (1) mucocutaneous candidiasis; (2) autoimmune tissue destruction; (3) ectodermal dystrophy. The disease is caused by mutations in a single ... ...

Abstract	Autoimmune polyglandular syndrome type 1 (APS1) is characterized by a variable combination of disease components: (1) mucocutaneous candidiasis; (2) autoimmune tissue destruction; (3) ectodermal dystrophy. The disease is caused by mutations in a single gene called APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal-dystrophy) or AIRE (autoimmune regulator) coding for a putative transcription factor featuring two zinc-finger (PHD-finger) motifs. APS1 shows a penetrance of 100%, lack of female preponderance and lack of association with HLA-DR. Typically, onset of APS1 occurs in childhood and multiple autoimmune manifestations evolve throughout lifetime. Organ-specific autoantibodies associated with hypoparathyroidism, adrenal and gonadal failures, IDDM, hepatitis and vitiligo are discussed, and autoantibody patterns in APS1 patients are compared with autoantibodies in APS type 2 (APS2). APS2 is characterized by adult onset adrenal failure associated with IDDM and/or hyperthyroidism. APS2 is believed to be polygenic, characterized by dominant inheritance and association with HLA DR3.
MeSH term(s)	Adrenal Insufficiency/etiology ; Adult ; Diabetes Mellitus, Type 1/etiology ; Female ; Gonadal Disorders/etiology ; Hepatitis, Autoimmune/etiology ; Humans ; Hypoparathyroidism/etiology ; Infertility/etiology ; Male ; Polyendocrinopathies, Autoimmune/complications ; Polyendocrinopathies, Autoimmune/genetics ; Vitiligo/etiology
Language	English
Publishing date	1998-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	92115-4
ISSN	1878-0873 ; 0950-3528
ISSN (online)	1878-0873
ISSN	0950-3528
DOI	10.1016/s0950-3528(98)90136-1
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Article: Cytochromes P450 and uridine triphosphate-glucuronosyltransferases: model autoantigens to study drug-induced, virus-induced, and autoimmune liver disease.

Manns, M P / Obermayer-Straub, P

Hepatology (Baltimore, Md.)

1997 Volume 26, Issue 4, Page(s) 1054–1066

Abstract: Enzymes of phase I (cytochromes P450) and phase II (UDP [uridine diphosphate]-glucuronosyltransferases) of drug metabolism are targets of autoimmunity in the following chronic liver diseases of different etiology: 1)autoimmune hepatitis (AIH); 2) ... ...

Abstract	Enzymes of phase I (cytochromes P450) and phase II (UDP [uridine diphosphate]-glucuronosyltransferases) of drug metabolism are targets of autoimmunity in the following chronic liver diseases of different etiology: 1)autoimmune hepatitis (AIH); 2) hepatitis associated with the autoimmune polyendocrine syndrome type 1 (APS-1); 3) virus-induced autoimmunity; and 4) drug-induced hepatitis. AIH is diagnosed by the following: the absence of infection with hepatitis viruses; the presence of a threshold of relevant factors, including circulating autoantibodies, hypergammaglobulinemia, female sex (female/male ratio 4:1), human leukocyte antigen (HLA) B8, DR3, or DR4; and benefit from immunosuppression. Patients with autoimmune hepatitis type 2 (AIH-2) are characterized by antibodies directed against liver and kidney microsomes, by an early onset of autoimmune hepatitis, which is a more aggressive course of the disease, and by a higher prevalence of autoimmunity directed against other organs. The major target of autoimmunity in patients with AIH-2 is cytochrome P450 2D6. Epitope mapping experiments revealed four short linear epitopes on cytochrome P450 2D6, recognized by liver/kidney microsomal autoantibodies type 1 (LKM-1) in patients with AIH-2. In addition, about 10% of the patient sera contain autoantibodies that detect a conformational epitope on UDP-glucuronosyltransferases (UGTs) of family 1. Presently, LKM-1 autoantibodies are used as diagnostic markers for AIH-2. It is unclear whether these autoantibodies have a pathogenetic role. Hepatitis is found in some patients with APS-1. Presumably this also is an autoimmune liver disease. APS-1 patients with hepatitis may develop autoantibodies directed against microsomal P450 enzymes of the liver; however, these autoantibodies do not recognize cytochrome P450 2D6, but they do recognize cytochrome P450 1A2. Autoimmunity in patients with APS-1 usually is directed against several organs simultaneously, and several organ specific autoantibodies may exist. Interestingly, APS-1 patients may produce various anti-cytochrome P450 antibodies. In addition to the hepatic anti-cytochrome P450, 1A2 autoantibodies are directed against steroidogenic cytochromes P450, namely P450 c21, P450 scc, and P450 c17. These autoantibodies correlate with adrenal and ovarian failure and often these steroidal cell autoantibodies precede the manifestation of adrenal or ovarian dysfunction. Whether anti-P450 1A2 autoantibodies have a similar predictive value is not yet known. LKM autoantibodies are further found in association with chronic hepatitis C and D. In chronic hepatitis C, the major target of LKM autoantibodies is cytochrome P450 2D6. Predominantly, conformational epitopes are recognized by LKM-1 sera of patients with chronic hepatitis C. In 13% of patients with chronic hepatitis D, LKM-3 autoantibody is detectable. The target proteins are UGTs of family 1 and in a minority of sera UGTs of family 2. The epitopes are conformational. All hepatic diseases discussed earlier have in common that autoimmunity, which is directed against enzymes of drug metabolizing multigene families. Each disease is characterized by a specific pattern of autoantibodies, with apparently little overlap. For example, LKM-1 autoantibodies, which are directed against P450 2D6, seem to overlap between AIH and chronic hepatitis C. However, a close examination of these autoantibodies shows differences between LKM-1 autoantibodies from patients with chronic hepatitis C and with AIH. In AIH, LKM autoantibodies are more homogenous, titers are higher, and major autoepitopes on cytochrome P450 2D6 are small and linear. LKM autoantibodies in viral hepatitis C are more heterogeneous and there are multiple epitopes, many of which are conformational. These differences indicate the different mechanisms that are involved in the generation of autoimmunity. (ABSTRACT TRUNCATED)
MeSH term(s)	Amino Acid Sequence ; Animals ; Autoantigens/immunology ; Autoimmune Diseases/etiology ; Chemical and Drug Induced Liver Injury/immunology ; Cytochrome P-450 Enzyme System/immunology ; Glucuronosyltransferase/immunology ; Hepatitis, Viral, Human/immunology ; Humans ; Liver Diseases/etiology ; Liver Regeneration ; Molecular Sequence Data
Chemical Substances	Autoantigens ; Cytochrome P-450 Enzyme System (9035-51-2) ; Glucuronosyltransferase (EC 2.4.1.17)
Language	English
Publishing date	1997-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.510260438
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Article: Viral induction of autoimmunity: mechanisms and examples in hepatology.

Manns, M P / Obermayer-Straub, P

Journal of viral hepatitis

1997 Volume 4 Suppl 2, Page(s) 42–47

Abstract: Autoimmunity may be observed in chronic viral hepatitis, in particular hepatitis C and D. The hepatitis C virus (HCV) displays numerous interactions with the immune system. Hepatitis C virus induces a number of diseases of presumed autoimmune background, ...

Abstract	Autoimmunity may be observed in chronic viral hepatitis, in particular hepatitis C and D. The hepatitis C virus (HCV) displays numerous interactions with the immune system. Hepatitis C virus induces a number of diseases of presumed autoimmune background, like mixed cryoglobulinaemia, glomerulonephritis, panarthritis, arthritis, thyroiditis and skin lesions. On the other hand a number of autoantibodies are observed during the course of hepatitis C. Of particular interest are liver/kidney microsomal antibodies (LKM). Their occurrence in viral hepatitis may indicate an increased risk for treatment with interferons. LKM antibodies in chronic hepatitis C recognize several autoepitopes differing from those in autoimmune hepatitis. Hepatitis C-associated LKM antibodies are more heterogeneous. They recognize either conformational or several distinct linear autoepitopes on cytochrome P450 2D6; they may also react with other microsomal proteins. Apart from their molecular weight at 59 and 70 kDa these microsomal antigens are not yet identified. Another model of virus-induced autoimmunity in man is chronic hepatitis D which always requires co-infection with hepatitis B. Hepatitis D is known to be associated with a number of autoantibodies, amongst them LKM-3. LKM-3 antibodies have recently been shown to react with proteins of the UDP glucuronosyltransferase family (UGT). The main antigen is an autoepitope expressed on exon 2-5 of family 1 UGTs. Some hepatitis D sera recognize a minor second epitope on family 2 UGTs. It is interesting that hepatitis C patients recognize proteins of the cytochrome P450 family while hepatitis D sera react with UGTs. There seems to be little overlap between autoimmunity seen in hepatitis C and D as far as autoepitopes are concerned. LKM-3 antibodies against UGT 1 are also seen in a minority of patients with autoimmune hepatitis type 2. However, the autoimmune response against UGTs seen in autoimmune hepatitis differs from that observed in viral hepatitis. Autoantibodies in autoimmune liver disease are usually more homogenous and are directed against precise linear epitopes. Autoepitopes in autoimmune hepatitis usually represent conserved regions of these proteins, the antibody usually is inhibitory and antibody titres are very high. In contrast, autoantibodies in viral hepatitis are more heterogenous, recognize several linear and conformational epitopes; antibody titres are much lower. However, the major LKM autoantigen in chronic hepatitis C also is P450 2D6. Autoimmune hepatitis and autoimmunity in viral hepatitis must be distinguished clinically by all means due to the need for specific therapeutic interventions. These liver diseases may serve as models to study virus induced autoimmunity and autoimmune disease in man.
MeSH term(s)	Autoimmunity/immunology ; Chemical and Drug Induced Liver Injury/immunology ; Gastroenterology ; Hepatitis C, Chronic/immunology ; Hepatitis C, Chronic/physiopathology ; Hepatitis D, Chronic/immunology ; Hepatitis D, Chronic/physiopathology ; Humans ; Polyendocrinopathies, Autoimmune/immunology
Language	English
Publishing date	1997
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1212497-7
ISSN	1365-2893 ; 1352-0504
ISSN (online)	1365-2893
ISSN	1352-0504
DOI	10.1111/j.1365-2893.1997.tb00179.x
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Article: Autoimmunity in hepatitis C and D virus infection.

Strassburg, C P / Obermayer-Straub, P / Manns, M P

Journal of viral hepatitis

1996 Volume 3, Issue 2, Page(s) 49–59

Abstract: A large number of viruses are capable of inducing acute or chronic hepatitis. The syndrome of chronic hepatitis encompasses not only viral but also autoimmune liver diseases. The hepatitis C virus, and recently also the hepatitis D virus have been found ... ...

Abstract	A large number of viruses are capable of inducing acute or chronic hepatitis. The syndrome of chronic hepatitis encompasses not only viral but also autoimmune liver diseases. The hepatitis C virus, and recently also the hepatitis D virus have been found to be associated with an array of autoimmune syndromes, diseases and markers of autoimmunity. The relationship of hepatotropic virus infection and the immune system leading to virus-associated autoimmunity, and its distinction from genuine autoimmune disease represents a fascinating field of research. Clinically, the differentiation between autoimmune liver diseases, virus infection and virus-associated autoimmunity is difficult and epidemiological evaluations have not come up with universally applicable and valid classification criteria. However, both autoimmune liver diseases and viral hepatitis can readily be diagnosed and distinguished through precise and molecularly determined immunological testing systems. The overlap of both, virus-associated autoimmunity, is still at the centre of research activities aimed at establishing diagnostic and risk-assessment criteria. Studies of molecular autoantigens and autoepitopes have begun to define the differences of the B-cell response in autoimmune disease and virus-associated autoimmunity. This provides data that may contribute to the safe application of therapeutic strategies as different as immunosuppression and interferon-alpha (IFN-alpha). The present review focuses on the clinical, epidemiological and molecular aspects of these disease entities.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Autoimmunity/immunology ; Hepatitis C/immunology ; Hepatitis D/immunology ; Humans
Chemical Substances	Autoantibodies ; anti-liver kidney microsome antibody
Language	English
Publishing date	1996-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1212497-7
ISSN	1365-2893 ; 1352-0504
ISSN (online)	1365-2893
ISSN	1352-0504
DOI	10.1111/j.1365-2893.1996.tb00081.x
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Article: Cytochrome P450 enzymes and UDP-glucuronosyltransferases as hepatocellular autoantigens.

Obermayer-Straub, P / Manns, M P

Molecular biology reports

1996 Volume 23, Issue 3-4, Page(s) 235–242

Abstract: Cytochromes P450 and UDP-Glucuronosyltransferases (UGT) are targets of microsomal autoantibodies in liver and kidney (LKM). LKM autoantibodies are observed in autoimmune hepatitis, in some patients with viral hepatitis, drug-induced hepatitis and ... ...

Abstract	Cytochromes P450 and UDP-Glucuronosyltransferases (UGT) are targets of microsomal autoantibodies in liver and kidney (LKM). LKM autoantibodies are observed in autoimmune hepatitis, in some patients with viral hepatitis, drug-induced hepatitis and autoimmune hepatitis as disease component of the autoimmune polyglandular syndrome type 1 (APS-1). In autoimmune hepatitis LKM antibodies are markers of autoimmune hepatitis type 2. The major target of LKM-1 antibodies is cytochrome P450 2D6; a second less frequent target was the described UGTs of family 1. In autoimmune hepatitis LKM-1 autoantibodies are usually directed against small linear epitopes. LKM autoantibodies are also associated with infection with hepatitis viruses C and D. In hepatitis C about 1-2% of patients develop LKM-1 autoantibodies. About 60% of these autoantibodies are conformation dependent. The presence of LKM autoantibodies in hepatitis C may be associated with an increased risk in interferon treatment. LKM-3 autoantibodies are found in about 8% of patients with hepatitis D and are directed against conformational epitopes. Patients treated with certain drugs may develop drug induced hepatitis. In hepatitis induced by tienilic acid, tienilic acid is activated by and covalently bound to cytochrome P450 2C9. Activation of the immune system results in the formation of autoantibodies against cytochrome P450 2C9 (LKM-2) and infiltration of the liver with immune cells. A similar mechanism has been described for dihydralazine induced hepatitis, where autoantibodies are directed against P450 1A2 (LM). Autoantibodies directed against cytochrome P450 1A2 also are found in patients suffering from hepatitis as a disease component of APS-1.
MeSH term(s)	Animals ; Autoantigens ; Autoimmune Diseases/immunology ; Cytochrome P-450 Enzyme System/immunology ; Glucuronosyltransferase/immunology ; Humans ; Liver Diseases/immunology
Chemical Substances	Autoantigens ; Cytochrome P-450 Enzyme System (9035-51-2) ; Glucuronosyltransferase (EC 2.4.1.17)
Language	English
Publishing date	1996
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/bf00351174
Database	MEDical Literature Analysis and Retrieval System OnLINE

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