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. 2019 Mar 20;2019:8086257. doi: 10.1155/2019/8086257

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.