Combined analysis of polymorphisms of the tumor necrosis factor-alpha and interleukin-10 promoter regions and polymorphic xenobiotic metabolizing enzymes in psoriasis.

Environmental and genetic factors are thought to interact in the manifestation of psoriasis, but knowledge about the involved genes and antigens is incomplete. This study has focused on the association between psoriasis and inherited variations in xenobiotic metabolism and cytokine production as two components that may influence cutaneous immune responses to foreign substances. Polymorphisms of N-acetyltransferase 2, glutathione S-transferases T1 and M1, and promoter polymorphisms of the genes encoding for tumor necrosis factor-alpha and interleukin-10 were investigated in 151 Caucasian patients with psoriasis (100 with type I and 51 with type II psoriasis) and in 123 healthy controls. Polymorphisms were detected by polymerase chain reaction-based methods, restriction enzyme analysis, and direct sequencing. There were no significant differences in the distribution of enzyme polymorphisms or point mutations at position -1082 of the interleukin-10 promoter between the psoriasis groups and the control group. The G-->A polymorphism at position -238 of the tumor necrosis factor-alpha promoter (TNF alpha-238*A allele) was more common in type I psoriasis (27%) than in the controls [9.8%; odds ratio 3.4 (95% confidence interval 1.6-7.2); p = 0.0012; pcorr = 0.018]. Surprisingly, this overrepresentation of the tumor necrosis factor alpha-238*A allele was observed in male patients [4.1 (1.5-11.0); p = 0.0046; pcorr = 0.064] but not in female patients [1.8 (0.5-6.5); p = 0.5]. The G-->A polymorphism at position -308 of the tumor necrosis factor-alpha promoter was less frequent in type I psoriasis (23%) compared with controls (35.7%), although the negative association was weak [0.54 (0.3-0.97); p = 0.041; pcorr = not significant]. The distribution of the TNF alpha-238*A and TNF alpha-238*A alleles was similar in type II patients and controls. Our results suggest that male carriers of the G-->A polymorphism at position -238 of the tumor necrosis factor-alpha promoter are at an increased risk to develop early-onset psoriasis.

[1]  C. Garbe,et al.  Treatment of psoriasis with interleukin-10. , 1998, The Journal of investigative dermatology.

[2]  Paul Wordsworth,et al.  Interleukin-10 microsatellite polymorphisms and IL-10 locus alleles in rheumatoid arthritis susceptibility , 1998, The Lancet.

[3]  R. Westendorp,et al.  Interleukin 10 secretion in relation to human IL-10 locus haplotypes. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[4]  P. Barnes,et al.  Haplotype associated with low interleukin-10 production in patients with severe asthma , 1998, The Lancet.

[5]  J. Lanchbury,et al.  Interleukin-10 promoter polymorphisms in Southern Chinese patients with systemic lupus erythematosus. , 1998, Arthritis and rheumatism.

[6]  D. Tillman,et al.  Genetics of psoriasis: paternal inheritance and a locus on chromosome 6p. , 1998, The Journal of investigative dermatology.

[7]  J. Geier,et al.  Genotype and phenotype of N‐acetyltransferase 2 (NAT2) polymorphism in patients with contact allergy , 1998, Contact Dermatitis.

[8]  M. Walker,et al.  Tumour necrosis factor-alpha gene promoter polymorphism and decreased insulin resistance , 1998, Diabetologia.

[9]  W Sterry,et al.  IL-10 is a key cytokine in psoriasis. Proof of principle by IL-10 therapy: a new therapeutic approach. , 1998, The Journal of clinical investigation.

[10]  F. Heule,et al.  Delayed‐type hypersensitivity to contact allergens in psoriasis , 1998 .

[11]  E. Olasz,et al.  Demonstration and functional analysis of IL-10 receptors in human epidermal cells: decreased expression in psoriatic skin, down-modulation by IL-8, and up-regulation by an antipsoriatic glucocorticosteroid in normal cultured keratinocytes. , 1997, Journal of immunology.

[12]  S. Ahmed,et al.  Polymorphism in the tumor necrosis factor‐α promotor region and in the heat shock protein 70 genes associated with malignant tumors , 1997, Cancer.

[13]  E. Märker-Hermann,et al.  A TNF-α Promoter Polymorphism Is Associated with Juvenile Onset Psoriasis and Psoriatic Arthritis , 1997 .

[14]  T. Henseler,et al.  Genetics of psoriasis. , 1997, Archives of dermatological research.

[15]  D. Grant,et al.  Human acetyltransferase polymorphisms. , 1997, Mutation research.

[16]  H. Mcdevitt,et al.  Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[17]  R. Bayoumi,et al.  Polymorphic N-acetyltransferase (NAT2) genotyping of Emiratis. , 1997, Pharmacogenetics.

[18]  M. Lazarus,et al.  An investigation of polymorphism in the interleukin-10 gene promoter. , 1997, European journal of immunogenetics : official journal of the British Society for Histocompatibility and Immunogenetics.

[19]  J. Brockmöller,et al.  Deficiency of glutathione S-transferases T1 and M1 as heritable factors of increased cutaneous UV sensitivity. , 1997, The Journal of investigative dermatology.

[20]  O. Majdic,et al.  Molecular and functional characteristics of dendritic cells generated from highly purified CD14+ peripheral blood monocytes. , 1996, Journal of immunology.

[21]  E. Fisher,et al.  Evidence that a locus for familial psoriasis maps to chromosome 4q , 1996, Nature Genetics.

[22]  D. Niederwieser,et al.  Generation of mature dendritic cells from human blood. An improved method with special regard to clinical applicability. , 1996, Journal of immunological methods.

[23]  J. Brockmöller,et al.  Homozygous rapid arylamine N-acetyltransferase (NAT2) genotype as a susceptibility factor for lung cancer. , 1996, Cancer research.

[24]  W. Sterry,et al.  Familial juvenile onset psoriasis is associated with the human leukocyte antigen (HLA) class I side of the extended haplotype Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0303: a population- and family-based study. , 1996, The Journal of investigative dermatology.

[25]  J. Schröder,et al.  Co-localized overexpression of GRO-alpha and IL-8 mRNA is restricted to the suprapapillary layers of psoriatic lesions. , 1996, The Journal of investigative dermatology.

[26]  W. R. Lamb,et al.  A genetic marker of high TNF-α production in heart transplant recipients , 1995 .

[27]  C. Elmets,et al.  Metabolic requirements for induction of contact hypersensitivity to immunotoxic polyaromatic hydrocarbons. , 1995, Journal of immunology.

[28]  F. Pociot,et al.  Functional Analysis of a New Polymorphism in the Human TNF α Gene Promoter , 1995, Scandinavian journal of immunology.

[29]  J. Brockmöller,et al.  Arylamine N-acetyltransferase (NAT2) mutations and their allelic linkage in unrelated Caucasian individuals: correlation with phenotypic activity. , 1995, American journal of human genetics.

[30]  A. Fryer,et al.  Susceptibility to ulcerative colitis and Crohn's disease: interactions between glutathione S-transferase GSTM1 and GSTT1 genotypes. , 1995, Clinica chimica acta; international journal of clinical chemistry.

[31]  J. Simon,et al.  Rapid purification of human Langerhans cells using paramagnetic microbeads , 1995, Experimental dermatology.

[32]  T. Mosmann,et al.  IL-10 inhibits cytokine production, vascular leakage, and swelling during T helper 1 cell-induced delayed-type hypersensitivity. , 1994, Journal of immunology.

[33]  R. Strieter,et al.  Keratinocyte interleukin-10 expression is upregulated in tape-stripped skin, poison ivy dermatitis, and Sezary syndrome, but not in psoriatic plaques. , 1994, Clinical immunology and immunopathology.

[34]  Franco Ameglio,et al.  Correlated increases of tumour necrosis factor‐α, interleukin‐6 and granulocyte monocyte‐colony stimulating factor levels in suction blister fluids and sera of psoriatic patients relationships with disease severity , 1994, Clinical and experimental dermatology.

[35]  A. Bowcock,et al.  Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q. , 1994, Science.

[36]  H. Bolt,et al.  Human glutathione S-transferase theta (GSTT1): cDNA cloning and the characterization of a genetic polymorphism. , 1994, The Biochemical journal.

[37]  T. Griffith,et al.  Regulation of contact hypersensitivity by interleukin 10 , 1994, The Journal of experimental medicine.

[38]  D. Wallach,et al.  Elevated tumour necrosis factor‐alpha (TNF‐α) biological activity in psoriatic skin lesions , 1994, Clinical and experimental immunology.

[39]  James T. Elder,et al.  The genetics of psoriasis. , 1994, Journal of the American Academy of Dermatology.

[40]  W. Jochum,et al.  T cells involved in psoriasis vulgaris belong to the Th1 subset. , 1994, The Journal of investigative dermatology.

[41]  M. Yamamura,et al.  The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response. , 1993, The Journal of investigative dermatology.

[42]  W. Sterry,et al.  Oligonucleotide typing reveals association of type I psoriasis with the HLA-DRB1*0701/2, -DQA1*0201, -DQB1*0303 extended haplotype. , 1993, The Journal of investigative dermatology.

[43]  C. Wolf,et al.  Deduced amino acid sequence, gene structure and chromosomal location of a novel human class Mu glutathione S-transferase, GSTM4. , 1993, The Biochemical journal.

[44]  F. Pociot,et al.  An allelic polymorphism within the human tumor necrosis factor alpha promoter region is strongly associated with HLA A1, B8, and DR3 alleles , 1993, The Journal of experimental medicine.

[45]  F. Perera,et al.  Genetic monitoring of human polymorphic cancer susceptibility genes by polymerase chain reaction: application to glutathione transferase mu. , 1992, Environmental health perspectives.

[46]  E. Thompson,et al.  Performing the exact test of Hardy-Weinberg proportion for multiple alleles. , 1992, Biometrics.

[47]  R. Happle,et al.  Psoriasis vulgaris, fetal growth, and genomic imprinting. , 1992, American journal of medical genetics.

[48]  V. Dixit,et al.  Keratinocytes as initiators of inflammation , 1991, The Lancet.

[49]  V. Dixit,et al.  Marked synergism between tumor necrosis factor-alpha and interferon-gamma in regulation of keratinocyte-derived adhesion molecules and chemotactic factors. , 1990, The Journal of clinical investigation.

[50]  K. Matsushima,et al.  Production of interleukin-8 by human dermal fibroblasts and keratinocytes in response to interleukin-1 or tumour necrosis factor. , 1989, Immunology.

[51]  W. Pearson,et al.  Hereditary differences in the expression of the human glutathione transferase active on trans-stilbene oxide are due to a gene deletion. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[52]  E. Christophers,et al.  Psoriasis of early and late onset: characterization of two types of psoriasis vulgaris. , 1985, Journal of the American Academy of Dermatology.

[53]  D. Grant,et al.  A simple test for acetylator phenotype using caffeine. , 1984, British journal of clinical pharmacology.

[54]  S. Boyce,et al.  Calcium-regulated differentiation of normal human epidermal keratinocytes in chemically defined clonal culture and serum-free serial culture. , 1983, The Journal of investigative dermatology.

[55]  J. Karvonen,et al.  Psoriasis and HLA‐Cw6 , 1980, The British journal of dermatology.

[56]  E. Jawetz,et al.  A clinical evaluation , 1961 .

[57]  W. Sterry,et al.  Tumor necrosis factor-alpha gene polymorphism in psoriasis. , 1997, Experimental and clinical immunogenetics.

[58]  G. Schuler,et al.  Generation of mature dendritic cells from human blood. An improved method with special regard to clinical applicability. , 1997, Advances in experimental medicine and biology.