Volume 12 Supplement 1

Abstracts from the 1st Annual Meeting of the Scottish Society of Cytomics (SCC) 2014. "Translational Cytometry from Bench to Bedside"

Open Access

Deletion of myeloid-PTP1B decreases MHC Class I expression and peptide presentation through an IL-10 dependent mechanism in response to LPS challenge

  • Samantha Le Sommer1Email author,
  • Cristina Martin-Granados1 and
  • Mirela Delibegovic1
Journal of Inflammation201512(Suppl 1):P1

https://doi.org/10.1186/1476-9255-12-S1-P1

Published: 16 April 2015

Protein Tyrosine Phosphatase 1B (PTP1B) inhibition is a target in the treatment of type 2 Diabetes Mellitus, and as such PTP1B inhibitors are in Phase II clinical trials. Previously our laboratory demonstrated that myeloid-specific deletion of PTP1B (LysM PTP1B) results in an increase in systemic IL-10 secretion and expression. In the current work we investigated how PTP1B deficiency affects the activation phenotype of murine macrophages in response to inflammatory stimuli. We demonstrate that myeloid-specific PTP1B deletion results in a decrease in expression of MHC Class I, along with co-stimulatory molecules CD80 and CD40. Interaction assays reveal a defect in the cells’ ability to activate reporter B3Z T cells. Myeloid-specific PTP1B deletion increases the percentage of bone-marrow-derived-macrophages (BMDMs) positive for IL-10 which is associated with a decrease in iNOS production. Western blotting analysis demonstrated hyperphosporylation of ERK1/2 which has been suggested before to improve access to the IL-10 promoter. This provides evidence to suggest that myeloid-PTP1B deletion decreases MHC Class I expression and peptide presentation through an IL-10-dependent mechanism.

Authors’ Affiliations

(1)
Institute of Medical Sciences (IMS) School of Medical Sciences, University of Aberdeen

Copyright

© Le Sommer et al; licensee BioMed Central Ltd. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Advertisement