Studies in an experimental model of progressive TB in BALB/c mice showed that at the time of maximal protective activity mediated by high production of IFN-γ, TNF-α, and IL-1β (day 21 after infection), there is a strong activation of the HPA axis mediated by high production of CRH in the hypothalamus and adrenal hyperplasia with high serum concentrations of corticosterone. Here, IL1B is linked to tuberculosis.