FOXP3 and tuberculosis: In addition, increased IL-4 (i) impaired antimicrobial activity due to reduced TNF-α-mediated apoptosis of infected cells and decreased activity of iNOS (and therefore decreased levels of nitrogen and oxygen intermediates), (ii) increased iron availability for intracellular Mtb, and (iii) increased proliferation of FOXP3+ regulatory T cells, favoring the immunopathogenesis of TB [45].