**6. Psoriasis**

Psoriasis is a chronic, complex autoimmune disease with characteristic reddish patches covered by silvery-white scales. It affects approximately 120–180 million people worldwide [45]. The prevalence of psoriasis varies significantly depending mainly on race, geographical location, genetics, environmental factors, and ethnicity [46–50].

The etiology of psoriasis involves both genetic and environmental factors indicating a multifactorial nature. Moreover, a number of characteristic features of psoriasis are also found in other autoimmune diseases indicating a common etiology [51, 52].

#### *The Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22) Gene Polymorphism… DOI: http://dx.doi.org/10.5772/intechopen.90836*

Though the pathogenesis of psoriasis and comorbidities has been studied at the molecular level and a number of gene loci have been associated with susceptibility/ severity of psoriasis [50–53], genes identified till date to be associated with it do not fully account for it. Psoriasis is highly heritable, and it has been suggested in several association studies that skin barrier function, innate and adaptive immunity, and gene-gene and gene-environment interactions are involved in the pathogenesis of psoriasis [52].

Recently an association of T-allele of the PTPN22 C1858T with susceptibility to psoriasis in Saudi population was reported (**Table 3**) [53]. Earlier it has been suggested that *PTPN22* may be among the true psoriasis susceptibility risk genes [54]. However, another study analyzed 15 SNPs from 7 putative psoriasis-risk genes and could not find any significant association of PTPN22 C1858T polymorphism with psoriasis. On the other hand, they found a significant association with another polymorphism (rs3789604) in *PTPN22* gene and suggested that *PTPN22* is one of the significant risk genes for psoriasis [55]. Chen and Chang [56] reported a strong association of PTPN22 + 1858T allele with PsA but no association with psoriasis and suggested that attention should be given to the studies dealing with geneenvironment interaction besides keeping in consideration the clinical heterogeneity of the disease and population stratification.

Earlier Hüffmeier et al. [57] found gender variations in susceptibility of PTPN22 (+1858T allele) with psoriasis and suggested that other susceptibility locus/loci within noncoding regions of *PTPN22* or its proximity might exist and act independently as a risk factor. They excluded the direct link of T-allele in psoriasis susceptibility in German psoriasis patients.
