Table 1.
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.