Table 1.

Beneficial Effects of DHEA in Tuberculosis.

DHEA	References
Modulates the functional capacity of M. tuberculosis-stimulated dendritic cells favoring the expression of MHC I, MHC II, CD86, and the phosphorylation of ERK1 while augmenting and reducing the IL-12 and IL10 production, respectively. This further leads to a better specific T cell performance in terms of proliferation and IFN-γ production.	(48)
Induces MAPK activation and improves the performance of M. tuberculosis-exposed DCs in terms, of antigen-presenting activity, and T cell stimulation. This may favor the development of Th1 responses, crucial for the protective immune response to mycobacteria.	(48)
Increases IL-1β levels and promotes the induction of autophagy accompanied by a decrease in M. tuberculosis growth in cultured macrophages derived from THP1 cells, even in the presence of cortisol	(49)
Causes a drop in the bacterial count and prolonged survival of BALB/c mice with experimental TB. These effects correlate with the appearance of cellular infiltrates rich in cells expressing IL-2, IL-1β, and TNF-α, as well as an increase in the development of granulomas and suppression of areas affected by pneumonia	(51, 52)
Induces CD4 Th1 cells and macrophage activation through direct activity, and by also suppressing the local production of corticosterone in the lungs in BALB/c mice with experimental TB	(54)
Results in a respectively increased and decreased Th1 and Th2 cytokine production along with a better Mtb-driven lymphoproliferation in BALB/c mice with experimental TB, when given in combination with glucocorticoids.	(55, 56)
The sulfated form (DHEAS) results in a better production of specific IgG and IFN-γ in young mice immunized with mycHSP70 antigen, but not in the old ones.	(57)
The 16α-bromoepiandrosterone synthetic (DHEA derivative that does not enter sex steroid pathways) inhibits bacterial proliferation and increases the expression of TNF-a, IFN-γ, and iNOS while decreasing the expression of IL-4 in BALB/c mice with active TB	(58)

HDB-2, human defensin beta 2; HBD-3, Human defensin beta 3; mycHSP70, Mycobacterium tuberculosis heat shock protein 70; iNOS, inducible nitric oxide synthase.