Regulation of the human immune response during tuberculosis.

Pulmonary tuberculosis is characterized by depression of purified protein derivative-stimulated (PPD-stimulated) blastogenesis in peripheral blood mononuclear cells (PBMCs) as well as decreased production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). Circulating T cells and monocytes (MNs) are nonspecifically activated in situ. PPD directly stimulates the primed MNs from patients with tuberculosis (TB) to overproduce a panoply of cytokines including transforming growth factor-beta (TGF-beta) and IL-10, which serve to depress PPD-stimulated blastogenesis and cytokine expression. Cross-modulation by these immunosuppressive MN products is superimposed on a primary T cell abnormality that persists for at least 12 months after the diagnosis of TB and involves apoptotic mechanisms.