Exploring the pathways underlying cancer immune evasion
Tumours can inhibit the antitumour immune response by disrupting the balance governing the steps of the cancer immunity cycle through multiple mechanisms. The goal of cancer immunotherapy research is to understand these mechanisms to counteract the tumour's ability to suppress the immune response. These pathways may include1,2
- Stimulatory factors that promote the immune response against cancer
- Inhibitory factors that keep the cycle in check to prevent autoimmunity
Stimulatory and inhibitory factors involved in the cancer immunity cycle1,3
ATP=adenosine triphosphate; BTLA=B- and T-lymphocyte attenuator; CDN=cyclic dinucleotide; CSF-1R=colony-stimulating factor 1; CTLA4=cytotoxic T-lymphocyte antigen-4; CXCL/CCL=chemokine motif ligands; GITR=glucocorticoid-induced TNFR family-related gene; HMGB1=high-mobility group protein B1; HVEM=herpes virus entry mediator; ICAM1=intracellular adhesion molecule 1; IDO=indoleamine 2,3-dioxygenase; IFN=interferon; IL=interleukin; LAG-3=lymphocyte-activation gene 3 protein; LFA1=lymphocyte function-associated antigen-1; MIC=MHC class I polypeptide-related sequence protein; PD-L1=programmed death-ligand 1; TGF=transforming growth factor; TIM-3=T cell immunoglobulin domain and mucin domain-3; TLR=toll-like receptor; TNF=tumour necrosis factor; VEGF=vascular endothelial growth factor; VISTA=V-domain Ig suppressor of T cell activation.
- Chen DS, Mellman I. Oncology meets immunology: the cancer-immunity cycle. Immunity. 2013;39:1-10. PMID: 23890059
- Chen DS, Irving BA, Hodi FS. Molecular pathways: next-generation immunotherapy—inhibiting programmed death-ligand 1 and programmed death-1. Clin Cancer Res. 2012;18:6580-6587. PMID: 23087408
- Data on file. Genentech, Inc.