Delibegovic, Mirela

Le Sommer, Samantha

Martin-Granados, Cristina

Journal of Inflammation

English

PubMed

Samantha Le Sommer

Cristina Martin-Granados

Mirela Delibegovic

Crossref

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

Aberdeen University Research

POSTER PRESENTATION Open AccessDeletion of myeloid-PTP1B decreases MHC Class Iexpression and peptide presentation through anIL-10 dependent mechanism in response to LPSchallengeSamantha Le Sommer*, Cristina Martin-Granados, Mirela DelibegovicFrom 1st Annual Meeting of the Scottish Society of Cytomics (SCC) 2014. “Translational Cytometry fromBench to Bedside”Aberdeen, UK. 25 September 2014Protein Tyrosine Phosphatase 1B (PTP1B) inhibition is atarget in the treatment of type 2 Diabetes Mellitus, and assuch PTP1B inhibitors are in Phase II clinical trials. Pre-viously our laboratory demonstrated that myeloid-specificdeletion of PTP1B (LysM PTP1B) results in an increase insystemic IL-10 secretion and expression. In the currentwork we investigated how PTP1B deficiency affects theactivation phenotype of murine macrophages in responseto inflammatory stimuli. We demonstrate that myeloid-specific PTP1B deletion results in a decrease in expressionof MHC Class I, along with co-stimulatory moleculesCD80 and CD40. Interaction assays reveal a defect inthe cells’ ability to activate reporter B3Z T cells. Myeloid-specific PTP1B deletion increases the percentage ofbone-marrow-derived-macrophages (BMDMs) positive forIL-10 which is associated with a decrease in iNOS produc-tion. Western blotting analysis demonstrated hyperphos-porylation of ERK1/2 which has been suggested before toimprove access to the IL-10 promoter. This provides evi-dence to suggest that myeloid-PTP1B deletion decreasesMHC Class I expression and peptide presentation throughan IL-10-dependent mechanism.Published: 16 April 2015doi:10.1186/1476-9255-12-S1-P1Cite this article as: Le Sommer et al.: Deletion of myeloid-PTP1Bdecreases MHC Class I expression and peptide presentation through anIL-10 dependent mechanism in response to LPS challenge. Journal ofInflammation 2015 12(Suppl 1):P1.Submit your next manuscript to BioMed Centraland take full advantage of: • Convenient online submission• Thorough peer review• No space constraints or color figure charges• Immediate publication on acceptance• Inclusion in PubMed, CAS, Scopus and Google Scholar• Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit* Correspondence: r02sl13@abdn.ac.ukInstitute of Medical Sciences (IMS) School of Medical Sciences, University ofAberdeen, UKLe Sommer et al. Journal of Inflammation 2015, 12(Suppl 1):P1http://www.journal-inflammation.com/content/12/S1/P1© 2015 Le Sommer et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, andreproduction 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.

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POSTER PRESENTATION 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 Sommer*, Cristina Martin-Granados, Mirela Delibegovic
From 1st Annual Meeting of the Scottish Society of Cytomics (SCC) 2014. “Translational Cytometry from
Bench to Bedside”
Aberdeen, UK. 25 September 2014
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. Pre-
viously 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 produc-
tion. Western blotting analysis demonstrated hyperphos-
porylation of ERK1/2 which has been suggested before to
improve access to the IL-10 promoter. This provides evi-
dence to suggest that myeloid-PTP1B deletion decreases
MHC Class I expression and peptide presentation through
an IL-10-dependent mechanism.
Published: 16 April 2015
doi:10.1186/1476-9255-12-S1-P1
Cite this article as: Le Sommer et al.: Deletion of myeloid-PTP1B
decreases MHC Class I expression and peptide presentation through an
IL-10 dependent mechanism in response to LPS challenge. Journal of
Inflammation 2015 12(Suppl 1):P1.
Submit your next manuscript to BioMed Central
and take full advantage of: 
• Convenient online submission
• Thorough peer review
• No space constraints or color figure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at 
www.biomedcentral.com/submit
* Correspondence: r02sl13@abdn.ac.uk
Institute of Medical Sciences (IMS) School of Medical Sciences, University of
Aberdeen, UK
Le Sommer et al. Journal of Inflammation 2015, 12(Suppl 1):P1
http://www.journal-inflammation.com/content/12/S1/P1
© 2015 Le Sommer et al; licensee 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.


https://journal-inflammation.biomedcentral.com/track/pdf/10.1186/1476-9255-12-S1-P1?site=journal-inflammation.biomedcentral.com

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

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