Specific Nucleotide Sequence of HLA-C is Strongly Associated with psoriasis Vulgaris

Asahina, Akihiko; Akazaki, Shuichi; Nakagawa, Hidemi; Kuwata, Shoji; Tokunaga, Katsushi; Ishibashi, Yoshihiro; Juji, Takeo

doi:10.1111/1523-1747.ep12480361

Cited by 80 publications

(58 citation statements)

References 16 publications

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“…Interestingly these patients show replacement of a threonine residue for alanine at posi tion 73 of the HLA-C molecule. This is present in 81% of the Japanese patients as reported by Asahina et al [22] and 100% of our own patients [Henseler T, personal commun.]. Amino acid substitution of the epitope-binding pocket of HLA-C molecule was also noted in HLA-Cw3 and is pre sent in 20% o f normal (nonpsoriatic) persons.…”

Section: Im M Unogeneticssupporting

confidence: 76%

“…However. Cw7 is seen in another 17% of Japanese psoriasis patients in addition to Cw3 and Cwl I [21,22], Extended haplotypes for type-I psoriasis were subse quently observed by oligonucleotide typing. These consist of DRB 1*0701/2, -DQA 1*0201, and -DQB1*0303 in addi tion to Cw6 [7], These results support heterogeneity as re flected by identifying subtypes, one of which shows linkage to HLA loci on chromosome 6 possibly influencing age of onset.…”

Section: Im M Unogeneticsmentioning

confidence: 92%

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The Immunopathology of Psoriasis

Christophers

1996

Int Arch Allergy Immunol

126

101

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Psoriasis affects approximately 2% of the population in Western countries. Although clinically rather monomorphic, the disease presents with a number of phenotypically distinct and heterogeneous subgroups showing differences in their pathogenetic pathways. Patients with type I (early onset) psoriasis demonstrate inflammatory lesions with epidermal hyperproliferation and the presence of activated T cells as well as intraepidermal polymorphs as principal features. In contrast to pustular types of psoriasis, these patients show genetic susceptibility and strong association with MHC class I and class-I haplotypes. There is evidence for a T-cell-mediated pathomechanism leading to a large spectrum of regulatory mediators including cytokines and growth factors as well as lipid mediators which are abnormally expressed. Pathogenetically psoriasis shows features in common with chronic relapsing T-cell-mediated diseases including Crohn’s disease, rheumatoid arthritis and others.

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Section: Im M Unogeneticssupporting

confidence: 76%

Section: Im M Unogeneticsmentioning

confidence: 92%

The Immunopathology of Psoriasis

Christophers

1996

Int Arch Allergy Immunol

126

101

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“…Seventy-nine PV patients, all or part of whom were involved in the previously published studies [16, 17, 18, 19], were also included in this study and we had typed HLA-A, -B and -C loci serologically in those studies [16, 17, 18, 19]. …”

Section: Methodsmentioning

confidence: 99%

Lack of Association between the Promoter Polymorphisms at Positions –308 and –238 of the Tumor Necrosis Factor Alpha Gene and Psoriasis vulgaris in Japanese Patients

et al. 2003

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Background: Psoriasis features an increased level and activity of tumor necrosis factor α (TNF-α). The TNF-α gene has single nucleotide polymorphisms (SNPs) at positions –308 (–308G>A) and –238 (–238G>A) in the promoter region, and the –238G>A SNP has been reported to be associated with psoriasis vulgaris (PV) and psoriatic arthritis in Caucasians. Objective: To examine whether these SNPs are associated with susceptibility to PV in Japanese patients, we investigated the genotype and allele frequencies at each SNP in Japanese PV patients and in controls. Methods: We examined 163 PV patients and 96 healthy individuals. Genotyping was performed using the polymerase chain reaction-restriction fragment length polymorphism method. Results: No significant association between the genotypes or alleles of these SNPs and susceptibility to PV was observed. Conclusion: These SNPs themselves are not associated with susceptibility to PV in the Japanese.

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“…First, T-cell activation could occur through immunogenetically determined high-risk MHC molecule(s) binding to certain selfpeptides, which may be induced or overexpressed in psoriasis to a sufficient degree for T-cell activation (57)(58)(59). Second, microbial antigens, in particular superantigens (SAgs), may provide a stimulus for breaking through a subthreshold level of Tcell-receptor interaction in psoriatic skin (60)(61)(62).…”

Section: Epidermal Hyperplasia Is Maintained By a T-cellmediated Inflmentioning

confidence: 99%

Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

Terada

Ozawa

Tagami

2000

Experimental Dermatology

133

111

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A growing body of evidence has indicated that T-cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. In this review we present our own experimental results as well as those from the literature related to the pathomechanism of the development of inflammatory changes in psoriatic lesions. First of all it is important to acknowledge the fact that psoriatic lesions are not uniform as assumed by many authors but that they are actually rather heterogeneous both clinically and histologically even within the same plaques. Lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis, whose stimulated kertinocytes released several cytokines, which in turn enhance the activation state of T cells. Thus, they form a vicious cycle, a T-cell-mediated inflammationsustaining loop. Although the interaction between T-cell-mediated immunity and epidermal keratinocytes may well explain the maintenance of background ''chronic'' inflammatory changes diffusely observed throughout psoriatic lesions, it is not enough to explain the island-like, ''acute'' inflammatory changes observed within and at the border of the plaque lesions. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed and therapeutically recalcitrant areas of psoriatic lesions. They are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-a released by the stimulated keratinocytes, and particularly C5a/C5a des arg produced via the alternative complement pathway activation possibly on the surface of corneocytes. In this review, we emphasize that the accumulation of neurophils is not simply a passive event. We think that those stimulated neutrophils are able to influence not only the growth that may well explain the localized ''acute'' inflammatory changes scate-mail: terui/mail.cc.tohoku.ac.jp tered over the ''chronic'' psoriatic plaques as well as in the acutely inflamed lesions of pustular psoriasis.

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Specific Nucleotide Sequence of HLA-C is Strongly Associated with psoriasis Vulgaris

Cited by 80 publications

References 16 publications

The Immunopathology of Psoriasis

The Immunopathology of Psoriasis

Lack of Association between the Promoter Polymorphisms at Positions –308 and –238 of the Tumor Necrosis Factor Alpha Gene and Psoriasis vulgaris in Japanese Patients

Role of neutrophils in induction of acute inflammation in T‐cell‐mediated immune dermatosis, psoriasis: A neutrophil‐associated inflammation‐boosting loop

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