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IDO1 Signaling through GCN2 in a Subpopulation of Gr-1 + Cells Shifts the IFNγ/IL6 Balance to Promote Neovascularization
Journal article   Open access   Peer reviewed

IDO1 Signaling through GCN2 in a Subpopulation of Gr-1 + Cells Shifts the IFNγ/IL6 Balance to Promote Neovascularization

Souvik Dey, Arpita Mondal, James B DuHadaway, Erika Sutanto-Ward, Lisa D Laury-Kleintop, Sunil Thomas, George C Prendergast, Laura Mandik-Nayak and Alexander J Muller
Cancer immunology research, v 9(5), pp 514-528
May 2021
PMID: 33622713
url
https://doi.org/10.1158/2326-6066.CIR-20-0226View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Animals Cell Line, Tumor Disease Models, Animal Female Humans Indoleamine-Pyrrole 2,3,-Dioxygenase - genetics Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism Inflammation - metabolism Inflammation - pathology Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-6 - genetics Interleukin-6 - metabolism Mice Mice, Inbred BALB C Mice, Knockout Neoplasm Metastasis Neoplasms - etiology Neoplasms - metabolism Neoplasms - pathology Neovascularization, Pathologic - genetics Neovascularization, Pathologic - metabolism Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Signal Transduction
In addition to immunosuppression, it is generally accepted that myeloid-derived suppressor cells (MDSC) also support tumor angiogenesis. The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO1) has been implicated in promoting neovascularization through its positioning as a key regulatory node between the inflammatory cytokines IFNγ and IL6. Here, we report that within the heterogeneous expanse of Gr-1 MDSCs, both IDO1 expression and the ability to elicit neovascularization were associated with a minor subset of autofluorescent, CD11b cells. IDO1 expression was further restricted to a discrete, CD11c and asialo-GM1 double-positive subpopulation of these cells, designated here as IDVCs (IDO1-dependent vascularizing cells), due to the dominant role that IDO1 activity in these cells was found to play in promoting neovascularization. Mechanistically, the induction of IDO1 in IDVCs provided a negative-feedback constraint on the antiangiogenic effect of host IFNγ by intrinsically signaling for the production of IL6 through general control nonderepressible 2 (GCN2)-mediated activation of the integrated stress response. These findings reveal fundamental molecular and cellular insights into how IDO1 interfaces with the inflammatory milieu to promote neovascularization.

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Collaboration types
Industry collaboration
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Web of Science research areas
Immunology
Oncology
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