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Mapping of psoriasis to 17q terminus
  1. W-L Hwu1,*,
  2. C-F Yang2,3,*,
  3. C S J Fann3,
  4. C-L Chen3,
  5. T-F Tsai4,
  6. Y-H Chien1,
  7. S-C Chiang1,
  8. C-H Chen3,
  9. S-I Hung3,
  10. J-Y Wu3,
  11. Y-T Chen3,5
  1. 1Departments of Pediatrics and Medical Genetics, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan
  2. 2Graduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan
  3. 3Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
  4. 4Departments of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan
  5. 5Department of Pediatrics, Duke University Medical Center, Durham, NC, USA
  1. Correspondence to:
 Professor Yuan-Tsong Chen
 Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan;

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Psoriasis is a chronic, inflammatory, hyperproliferative disease of the skin, scalp, nails, and joints, with a prevalence of up to 2% in Caucasians1,2 but well under 1% in the Mongoloid races of the Far East.3 The disease varies in severity. Some patients display mild disease with isolated scaling erythematous plaques on the elbows or knees, whereas for others most of their cutaneous surface can be affected. At the cellular level, psoriasis is characterised by markedly increased epidermal proliferation and incomplete differentiation, elongation, dilation, and leakiness of the superficial plexus of dermal capillaries, and by a mixed inflammatory and immune cell infiltrate of the epidermis and papillary dermis.1,2 Dermal infiltrates comprised of T cells and macrophages typically appear in early lesions before epidermal changes.4 The therapeutic effect of immunosuppressive agents suggests psoriasis has a primary immune pathogenic basis.5

Susceptibility to the development of psoriasis is likely to have a significant genetic component. Accumulating evidence is consistent with the idea that psoriasis is a multifactorial disorder caused by the concerted action of multiple disease genes in a single individual and triggered by environmental factors.6 Some of these genes control the severity of a variety of diseases, via their regulation of the inflammatory and immune processes (severity genes), whereas others are unique to psoriasis (specific genes).

A number of genetic studies have sought to identify the psoriasis susceptibility loci. Associations between psoriasis and human lymphocyte antigen alleles were first described in 1990.7 Subsequently, genome-wide linkage scans have mapped psoriasis to several chromosomal regions including PSORS1 at 6p21,8,9 PSORS2 at 17q,8–10 PSORS3 at 4q,11 PSORS4 at 1q,12 PSORS5 at 3q,13 PSORS6 at 19p,14 and PSORS7 at 1p.15 Recently, the International Psoriasis Genetics Consortium reassessed these candidate …

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  • * These two authors contributed equally to this paper.

  • This work was supported by the National Science and Technology Program for Genomic Medicine from the National Science Council, Taiwan, and the Genomics and Proteomics Program from the Academia Sinica, Taiwan.

  • Conflict of interest: none declared.