Are other protein tyrosine phosphatases than PTPN22 associated with autoimmunity?

The discovery that a single amino acid substitution in the PTPN22 protein tyrosine phosphatase can predispose to so many autoimmune diseases (see chapters 2 and 3), even when present in a single copy, raises many questions regarding the broader significance of this observation. Is there something unique about PTPN22 or are genetic variants of other protein tyrosine phosphatases likely also associated with autoimmune disease? If so, will polymorphisms in other phosphatases be found in the same spectrum of diseases? Are protein tyrosine phosphatases like PTPN22 good drug targets for the treatment of human autoimmunity? In this review, I offer some basis for thinking about these questions.