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How do Tumors Actively Escape from Host Immunosurveillance?

  • REVIEW
  • Published:
Archivum Immunologiae et Therapiae Experimentalis Aims and scope

Abstract

The immunological background for the process of tumor growth is still obscure. However, our understanding of what happens could have important consequences, namely in the context of cancer immunotherapy. A tumor is able to grow in the host environment either because it is recognizable as normal tissue and tolerated by host immune cells, or because it can “escape” from host immunosurveillance. According to the second option the mechanisms of tumor recognition and consequent destruction are actively disturbed by such processes as: change of tumor immunogenicity, production of tumor-derived regulatory molecules, and interaction of cancer cells with tumor-infiltrating immune cells. The results of studies devoted to the problem of immunoregulation in the tumor environment seem to support the “escape” hypothesis.

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Abbreviations

TAA:

Tumor-associated antigens

ROI:

Reactive oxygen intermediates

NK:

Natural killer cells

NKT:

Natural killer T cells

CTL:

Cytotoxic T lymphocytes

IFN:

Interferon

STAT-1:

Signal transducer and activator of transcription-1

TGF:

Transforming growth factor

bFGF:

Basic fibroblast growth factor

FGF:

Fibroblast growth factor

PDGF:

Platelet-derived growth factor

EGF:

Epidermal growth factor

VEGF:

Vascular-endothelial growth factor

HIF-1α:

Hypoxia-inducible factor-1α

PGE2 :

Prostaglandin E2

IL:

Interleukin

MMPs:

Matrix metalloproteinases

PI3K:

Phosphoinositide 3-kinase

Akt:

Protein kinases B

MAPK:

Mitogen-activated protein kinase

CAFs:

Cancer-associated fibroblasts

TAMs:

Tumor-associated macrophages

NRP:

Neuropilin

MDSC:

Myeloid-derived suppressor cells

CCL:

Chemokine (C–C motif) ligand

CXCL:

Chemokine (C–X–C motif) ligand

HLA:

Human leukocyte antigen

MHC:

Major histocompatibility complex

NF-κB:

Nuclear factor-κB

KIR:

Killing inhibitory receptor

ILT:

Immunoglobulin-like transcript

DCs:

Dendritic cells

NKG2:

Activating receptor of NK cells

NKp44:

NK cell p44-related protein

CCR:

Chemokine (C–C motif) receptor

CXCR:

Chemokine (C–X–C motif) receptor

LMP:

Low-molecular mass polypeptide

MART-1/MelanA:

Melanoma-associated antigen recognized by T cells

IDO:

Indoleamine 2,3-dioxygenase

RCAS1:

Cancer antigen expressed on SiSo cells

TNF:

Tumor necrosis factor

TRAIL:

TNF-related apoptosis-inducing ligand

c-FLIP:

Fas-associated death domain-like interleukin-1 converting enzyme inhibitory protein

COX-2:

Cyclooxygenase-2

15-PGDH:

15-hydroxyprostaglandin dehydrogenase

NO:

Nitric oxide

TCR:

T cell receptor

MC:

Mast cells

RANTES:

Regulated on activation, normal T cell expressed and secreted

Tregs:

T regulatory cells

TILs:

Tumor-infiltrating lymphocytes

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Wilczyński, J.R., Duechler, M. How do Tumors Actively Escape from Host Immunosurveillance?. Arch. Immunol. Ther. Exp. 58, 435–448 (2010). https://doi.org/10.1007/s00005-010-0102-1

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