We have shown, in this experimental model of pulmonary TB, that by blocking TGF-β activity by the administration of its soluble receptor type 3 or betaglycan, while simultaneously suppressing PGE-2 production by the administration of niflumic acid, a specific cyclooxygenase type 2 (COX-2) blocker, we can produce a significant therapeutic benefit associated with restoration of the protective cytokine pattern (41). This evidence concerns the gene TGFB1 and pulmonary tuberculosis.