The Immunomodulatory Effect of Alpha-Lipoic Acid in Autoimmune Diseases

Table 1

Evidence of ALA on adaptive immune cells.

		T cell	B cell
Animal model	EAE	Decrease the number of Th17 and Th1 in CNS; Increase Treg numbers in spleen; Reduce migration.
	High fat diet mice	Recover transcriptional levels of the differentiation-related genes of jejunal T cells.	Restore transcriptional levels of BCR signaling pathway relating genes; Decrease the apoptotic percentage of splenic B lymphocytes.
	Atopic dermatitis	Suppress production of IFN-γ and IL-4 by CD4+T.	Reduce total serum IgE levels.
	Models of established atherosclerosis	Reduce T cell migration in response to chemokines.
	Endotoxemia mice		Increase the number of splenic B cells.
Patients	AIDS	Increase the number of Th cells; Improve the lymphocyte proliferation response; Ameliorate the impaired mitochondrial function of CD4^+T cells.
	Advanced cancer	Induce lymphocyte progression from G0/G1 to S phase.
	Jurkat T cells	Inhibit NF-κB activation induced by TNF; Reduce migration.
Normal human		Increase cAMP which affects proliferation and activation of T cells; Down-regulate the expression of CD4 molecules; Reduce migration.

ALA: α-lipoic acid.
EAE: experimental autoimmune encephalomyelitis.
Th17: T helper cell 17.
Th1: T helper cell 1.
CNS: central nervous system.
Treg: regulatory T cells.
BCR: B-cell receptor.
IFN-γ: interferon-γ.
AIDS: acquired immunodeficiency syndrome.
NF-κB: nuclear factor kappa B.
TNF: tumor necrosis factor.
cAMP: cyclic adenosine monophosphate.