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PTPN22 splice forms: a new role in rheumatoid arthritis

Lina-Marcela Diaz-Gallo and Javier Martin

Author Affiliations

Instituto de Parasitología y Biomedicina López-Neyra, CSIC (IPBLN-CSIC), Parque Tecnológico Ciencias de la Salud, Avenida del Conocimiento s/n 18100, Armilla, Granada, Spain

Genome Medicine 2012, 4:13  doi:10.1186/gm312

Published: 24 February 2012

Abstract

Genetic variation in the protein tyrosine phosphatase non-receptor type gene 22 (PTPN22, encoding lymphoid tyrosine phosphatase, LYP) influences the risk of developing multiple autoimmune diseases, but the underlying mechanisms are not completely understood. In a recent study published in Genome Medicine, Ronninger et al. showed that there are differences in the expression of PTPN22 isoforms between peripheral blood mononuclear cells from rheumatoid arthritis patients and those of healthy controls. This study provides new insights into the role of PTPN22 in autoimmune diseases.

Keywords:
Protein tyrosine phosphatase non-receptor type 22 (PTPN22); autoimmune diseases; rheumatoid arthritis; splice forms