Table 1.

Effects of micronutrients on neonatal immune response.

Nutrient	Target cells	Effect on development of immune system	Interactions in infection	Mechanism
Zinc	T cells, NK cells, B cells	Deficiency impairs immune response, ↓ hematopoiesis	Levels are rapidly depleted	Deficiency ↑ glucocorticoid ↓ pre T cell and B cells via Bcl-2 →apoptosis
		Lymphopenia, dermatitis, enteritis	Repletion ↑ recovery	Required for thymic hormone function
		↓ T thymus, bone marrow	Deficiency promotes infection	Required for activity of > 100 enzymes
		↓ antioxidant enzyme activity	Repletion reduces morbidity, mortality	Required for zinc finger dependent transcription factors
Iron	T cells, monocytes	Deficiency affects T and NK cell development, ↓ neutrophil oxidative burst activity and ↓IgG4	Anemia linked to HIV mortality	Promotes Th-2 response, ROS production
			Iron excess causes infection in genetically susceptible host	Promotes bacterial growth; deficiency ↓IL-2
			↑ HIV replication	Host polymorphisms and iron handling genes affect sequestration, pools; HFE gene regulates iron
Selenium	Monocytes, T cells, NK cells	Deficiency affects T and NK cell development	Improves survival in HIV infection	Antioxidant
		Deficiency suppresses antigen presentation	May enhance maternal HIV transmission	Affects IL-2 response, regulates NF kappa B
		Repletion ↑ T cell proliferation		May interact with viral genes
Vitamin A	T cells, NK cells, B cells	Promotes gut integrity	Deficiency ↑ infections and mortality from infections	Promotes Th-2 cytokine and IgA production
		Deficiency ↓ NK activity	Levels depleted in infection	Inducer for gut-homing of T cells
		Repletion improves gut integrity at weaning	Repletion ↑ recovery, reduces infection morbidity, mortality	IL-2 receptor beta, interferon regulatory factor, transcription factor mRNA Affects IL-12 and IL-10 production
Vitamin C	Phagocytes	Promotes phagocytic and NK activity	↑ response to strep infection	Decreases monocyte response to LPS
		Reduces stress IL-6 response	Reduces growth of H. pylori	Increases phagocytosis Increases NK activity
Vitamin D, 1,25-dihydroxy-vitamin D3	T cells, B cells, monocytes, macrophages, dendritic cells	Promotes gut integrity	Vitamin D deficiency promotes TB infection	Functions through a nuclear receptor, vitamin D receptor (VDR) which binds to response elements in target genes
		Vitamin D3 affects differentiation, maturation, and function of cells		Affects differentiation of monocytes and dendritic cells
		Vitamin D3 suppresses autoimmune disease in animal models		VDR polymorphisms regulate response to mycobacteria, hepatitis B, inflammatory bowel disease through TLR signaling
Vitamin E	T cells, B cells, monocytes	Maternal levels provide allergic protection	Deficiency may promote viral virulence	Modulates cyclic AMP response element binding proteins
		T cell proliferation and IL-2 response ↑ in vitro		Affects prostaglandin production
		Improves skin test response