|
CHS immune cell | CHS immune reaction | Plausible direct effect on tumor | Plausible immune suppression that may lead to tumor growth |
|
Hapten modification of epidermal cells → release of danger signals | Prostaglandin E2 (PGE2) release | Colon cancer growth [137] | MDSCs activation [116] |
ROS release | Angiogenesis through VEGF [138] | Nitration of T-cell-peptide-MHC interaction → T-cell suppression [116] |
ATP release → P2RX7 → NLRP3 activation | N/A | Decreased tumor responsiveness to vaccination [115] |
|
LCs and dDCs | TLR4 and 2 Stimulation | N/A | Immune evasion and myeloid cells to promote metastases [115, 116] |
|
Keratinocytes | IL-1β, IL-6, IL-18, and TNFα | N/A | MDSCs recruitment and infiltration → IL-10 production in tumor site [116] |
CXCL10 Upregulation | Angiogenesis [139] | N/A |
|
iNKT cells | IL-4 and IL-13 | N/A | MDSCs and M2MΦ recruitment and infiltration → IL-10 and TGFβ production in tumor site [116]; Suppression of tumor-specific CD8+ T-cells [140] |
|
Mast cells | CCL2 and CCL5 upregulation | N/A | TAMs (IL-10 high, IL-12 low, IL-1Rα high, and IL-1decoyR high) → IL-10, angiogenesis, tumor metastasis stimulation, TGFβ, TNFα, IL-1α [116]; MDSCs recruitment and infiltration → IL-10 production in tumor site [116] |
TNFα | Oxygen delivery to hypoxic tumor cells [116] | N/A |
CXCL2 | Melanoma cell proliferation [139] | N/A |
|
Neutrophils | CXCL1 and CXCL2 | Melanoma cell proliferation [116, 139] | N/A |
|
Hapten-specific T-regs | IL-10 | N/A | Effector T-cell suppression [141] |
CTLA-4 | N/A | CD8+ T-cell exhaustion [118] |
|