The protein tyrosine phosphatase PTPN22 negatively regulates presentation of immune complex derived antigens View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-08-23

AUTHORS

Fiona Clarke, Harriet A. Purvis, Cristina Sanchez-Blanco, Enrique Gutiérrez-Martinez, Georgina H. Cornish, Rose Zamoyska, Pierre Guermonprez, Andrew P. Cope

ABSTRACT

A C1858T single nucleotide polymorphism within PTPN22 (which encodes PTPN22R620W) is associated with an enhanced susceptibility to multiple autoimmune diseases including type 1 diabetes and rheumatoid arthritis. Many of the associated autoimmune diseases have an autoantibody component to their pathology. Fc receptors (FcRs) recognise autoantibodies when they bind to autoantigens and form immune complexes. After immune complex binding and receptor crosslinking, FcRs signal via Src and Syk family kinases, leading to antigen uptake, presentation and cytokine secretion. Ptpn22 encodes a protein tyrosine phosphatase that negatively regulates Src and Syk family kinases proximal to immunoreceptor signalling cascades. We therefore hypothesised that PTPN22 regulates immune complex stimulated FcR responses in dendritic cells (DCs). Bone marrow derived DCs (BMDCs) from wild type (WT) or Ptpn22-/- mice were pulsed with ovalbumin:anti-ovalbumin immune complexes (ova ICs). Co-culture with WT OT-II T cells revealed that ova IC pulsed Ptpn22-/- BMDCs have an enhanced capability to induce T cell proliferation. This was associated with an increased capability of Ptpn22-/- BMDCs to present immune complex derived antigens and to form ova IC dependent DC-T cell conjugates. These findings highlight PTPN22 as a regulator of FcR mediated responses and provide a link between the association of PTPN22R620W with autoantibody associated autoimmune diseases. More... »

PAGES

12692

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-31179-x

DOI

http://dx.doi.org/10.1038/s41598-018-31179-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1106199616

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30139951


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