Hapten-Induced Contact Hypersensitivity, Autoimmune Reactions, and Tumor Regression: Plausibility of Mediating Antitumor Immunity

Table 3

Contact hypersensitivity reactions that may lead to tumor growth.

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]

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