Vitamin-mediated cancer immune reprogramming: Context-dependent mechanisms and translational perspectives

Table 1 Context-dependent and bidirectional immunomodulatory effects of vitamins in cancer

Vitamin	Immune compartment	Potential anti-tumor effect	Potential tolerogenic/pro-tumor or context-dependent effect	Ref.
Vitamin A/retinoids	Macrophages	Promote macrophage activation and tumor-cell clearance	Retinoid signaling can also support tissue tolerance depending on context	[82,83]
	DCs	Promote DC differentiation and antigen presentation	RA signaling can promote tolerogenic DC phenotypes in some tissues	[24,84]
	T cells	Enhance LTαβ signaling and tumor-cell apoptosis	RA can influence T-cell differentiation toward regulatory phenotypes	[25,28]
Vitamin B5	Macrophages	Support phagocytosis and antigen presentation	Cancer-specific mechanistic evidence remains limited	[44,85]
Vitamin B2/B6/B9	NK cells	Support NK-cell cytotoxic function under adequate nutritional status	Immunological outcomes strongly depend on metabolic and cytokine context; cancer-specific data are sparse	[56,86]
Vitamin C	NK cells/T cells	Enhance NK-cell proliferation and CD8+ T-cell cytotoxicity in pre-clinical models	Antioxidant effects may be context-dependent and could theoretically blunt ROS-dependent therapies	[7,14]
Vitamin D	Macrophages	Enhance phagocytosis in selected pre-clinical contexts	Can promote tolerogenic macrophage/DC programs and suppress T-cell activation	[23,52]
Vitamin E	DCs	Enhance DC cross-presentation in pre-clinical tumor models	Antioxidant activity may interfere with ROS-dependent anti-tumor mechanisms in some contexts	[9,87]
Vitamin K	T cells/macrophages	Emerging pre-clinical evidence for tumor-cell and macrophage-related effects	Potential T-cell suppression and immunoregulatory effects; robust clinical cancer immunology evidence remains limited	[88,89]

DCs: Dendritic cells; LTαβ: Lymphotoxin αβ; RA: Retinoic acid; NK: Natural killer; ROS: Reactive oxygen species.