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Background: PTPN22 codifies for a protein-tyrosine-phosphatase (Lyp) involved in T cellreceptor signaling regulation. p53 is involved in immune related inflammation regulatingSTAT 1 and pro-inflammatory cytokines. Possible interaction between the two systemsconcerning the susceptibility to immune related disorders are therefore biologicallyplausible. In the present note we have searched for such interaction in type 1 diabetesmellitus and reviewed previous data from our laboratory.Methods: We have studied 287 children with type 1 diabetes, 129 non diabetic adultsubjects admitted to the Hospital for Coronary Artery Disease, 130 women withendometriosis and 256 healthy blood donors. PTPN22 and p53 codon 72 genotypes weredetermined by DNA analysis.Results: In all diseases the proportion of PTPN22 *T allele is higher in p53 *Pro allelecarriers than in p53*Arg/*Arg genotype. In *Arg/*Arg patients the proportion of *T allele carriers does not differ significantly from controls while in subjects carrying the *Pro alleleis higher in patients than in controls. A significant increase of Odds Ratio is observed onlyin presence of both *T and *Pro alleles suggesting a cooperative interaction.Conclusion: It has been suggested that the susceptibility to autoimmune disorders in thepresence of *T allele could be related to failure to delete auto reactive T cell duringintrathymic selection. *Pro allele variant with its strong transcriptional activity couldenhance the multiplication of such auto reactive T cell escaping intrathymic thusexplaining a significant increase of Odds Ratio in the presence of both factors .Thepresent observation could have relevance to identify individuals at high risk of clinicalmanifestations

Evidence of Interaction between PTPN22 and p53 codon 72 Polymorphisms on Susceptibility to Immune Related Diseases