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. 2019 Dec 13;11(12):2010. doi: 10.3390/cancers11122010

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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KRAS-induced immune-suppressive microenvironment. Mutant (mut)KRAS cells have been associated with decreased major histocompatibility class I (MHCI) expression, representing an impaired capacity to present antigens. Furthermore, the upregulation of programmed cell death ligand 1 (PD-L1) leads to immune evasion by inhibiting T-cell recognition. In these cells, the expression and secretion of several inflammatory cytokines is also recognized as being increased. Chemokine C-X-C ligand 3 (CXCL3) binds to its receptor chemokine C-X-C receptor 2 (CXCR2) on myeloid-derived suppressor cells (MDSCs) contributing to the maintenance and recruitment of these immune suppressive cells. In addition, granulocyte macrophage colony-stimulating factor (GM-CSF) is responsible for the accumulation of MDSCs in the tumor microenvironment. Moreover, the increased secretion of interleukin (IL)-10 and Transforming growth factor beta 1 (TGFβ1) induce the conversion of CD4+ CD25− T-cells into FOXP3+/CTLA4+/CD122+ T regulatory cells (Tregs) promoting immune suppression.