Exploring the Drug Repurposing Versatility of Valproic Acid as a Multifunctional Regulator of Innate and Adaptive Immune Cells

Table 2

Effects of valproic acid on some cellular elements of the immune response.

Cell	Observed effects	References
Monocytes	Reduction of proinflammatory cytokines	[49, 50]
	Reduction of surface molecules	[52]
Macrophages	Reduction of proinflammatory cytokines	[56, 58–61, 66, 76]
	Reduction of costimulatory molecules	[61]
	Reduction of ROS and NO	[57, 58, 63]
	Reduction of phagocytosis of extracellular pathogens	[63]
	Mycobacterium tuberculosis replication control	[64–67]
Dendritic cells	Reduction of proinflammatory cytokines	[59, 81, 82]
	Reduction of costimulatory molecules	[59, 79–82]
	Reduction of MHC-II	[82]
Neutrophils	Reduction of phagocytosis	[90]
	Reduction of chemotaxis	[90]
	Cellular arrest	[84]
	Apoptosis	[68]
Eosinophils	Eosinophilia in some clinical studies	[93–97]
Basophils	Reduction in total numbers in mouse autoimmune lymphoproliferative syndrome models	[99]
Mast cells	Reduction of cellular proliferation and viability	[100]
NK lymphocytes	Reduction of cellular proliferation	[109]
	Reduction of cytotoxic activity	[101–106]
Tγδ lymphocytes	Apoptosis	[110, 111]
B cells	Inhibition of differentiation of B cell into plasma cell	[112–115]
T CD4^+ lymphocytes	Reduction of cellular viability	[120, 129]
	Reduction in proinflammatory cytokines	[50, 124, 126, 128]
T CD8^+ lymphocytes	Reduction of cytotoxic activity	[116]
	Reduction of cellular viability	[120]
Treg lymphocytes	Increase of cellular proliferation	[122, 124, 125, 127, 135, 136]
	Increase in FoxP3 expression	[126, 133, 134]
	Increase of suppressor activity	[135–137]

ROS: reactive oxygen species; NO: nitric oxide; MHC-II: major histocompatibility molecule II.