The immunology of tuberculous pleurisy

Tuberculous pleurisy results when a subpleural nodule discharges mycobacterial antigens into the pleural space of a hypersensitive host. The clinical syndrome is a reflection of an in situ delayed-type hypersensitivity reaction in which plasma proteins are exuded into the pleural space and T-helper cells accumulate, proliferate, and produce, and release inflammatory mediators. The immune response initially contains the local infection, but in the absence of therapy, the host is at great risk of developing tuberculosis during the next 5 years. The focal accumulation of vigorously responsive T-helper cells and activated B cells in the pleural space may prove useful in identifying mycobacterial constituents which are immunogenic and possibly candidate vaccine antigens.