In keeping with the significantly reduced secretion of inflammatory and regulatory cytokines and loss of surface co-stimulatory molecules by BCG-TB1860-infected BMDC, splenocytes stimulated with these DC suffered almost complete loss of ability to secrete IFN-γ, a cytokine that again has been shown to be vital for anti-TB immunity [73], [74] as well as IL-2 and IL-17. Here, IL17A is linked to tuberculosis.