Peptide-based systems analysis of inflammation induced myeloid-derived suppressor cells reveals diverse signaling pathways

Author/Creator ORCID

Date

2016-05-19

Department

Program

Citation of Original Publication

Waeowalee Choksawangkarn, Lauren M. Graham, et.al, Peptide‐based systems analysis of inflammation induced myeloid‐derived suppressor cells reveals diverse signaling pathways, PROTEOMICS, Volume 16, Issue 13, DOI : https://doi.org/10.1002/pmic.201500102

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This is the peer reviewed version of the following article: Waeowalee Choksawangkarn, Lauren M. Graham, et.al, Peptide‐based systems analysis of inflammation induced myeloid‐derived suppressor cells reveals diverse signaling pathways, PROTEOMICS, Volume 16, Issue 13, DOI : https://doi.org/10.1002/pmic.201500102, which has been published in final form at https://doi.org/10.1002/pmic.201500102. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.

Abstract

A better understanding of molecular signaling between myeloid-derived suppressor cells (MDSC), tumor cells, T-cells, and inflammatory mediators is expected to contribute to more effective cancer immunotherapies. We focus on plasma membrane associated proteins, which are critical in signaling and intercellular communication, and investigate changes in their abundance in MDSC of tumor-bearing mice subject to heightened versus basal inflammatory conditions. Using spectral counting, we observed statistically significant differential abundances for 35 proteins associated with the plasma membrane, most notably the pro-inflammatory proteins S100A8 and S100A9 which induce MDSC and promote their migration. We also tested whether the peptides associated with canonical pathways showed a statistically significant increase or decrease subject to heightened versus basal inflammatory conditions. Collectively, these studies used bottom-up proteomic analysis to identify plasma membrane associated pro-inflammatory molecules and pathways that drive MDSC accumulation, migration, and suppressive potency.