Regulation of autoimmune and anti-tumour T-cell responses by PTPN22.
Rebecca J BrownlieRose ZamoyskaRobert J SalmondPublished in: Immunology (2018)
A number of polymorphisms in immune-regulatory genes have been identified as risk factors for the development of autoimmune disease. PTPN22 (that encodes a tyrosine phosphatase) has been associated with the development of several autoimmune diseases, including type 1 diabetes, rheumatoid arthritis and systemic lupus erythematosus. PTPN22 regulates the activity and effector functions of multiple important immune cell types, including lymphocytes, granulocytes and myeloid cells. In this review, we describe the role of PTPN22 in regulating T-cell activation and effector responses. We discuss progress in our understanding of the impact of PTPN22 in autoimmune disease in humans and mouse models, as well as recent evidence suggesting that genetic manipulation of PTPN22 expression might enhance the efficacy of anti-tumour T-cell responses.
Keyphrases
- systemic lupus erythematosus
- type diabetes
- rheumatoid arthritis
- dendritic cells
- multiple sclerosis
- disease activity
- mouse model
- regulatory t cells
- induced apoptosis
- transcription factor
- bone marrow
- cell cycle arrest
- metabolic syndrome
- long non coding rna
- cell proliferation
- ankylosing spondylitis
- interstitial lung disease
- genome wide analysis