Evaluation of interferon-γ, interferon-γ-inducing cytokines, and interferon-γ–inducible chemokines in tuberculous pleural effusions

Abstract

Tuberculous and malignant pleural effusions are representative of lymphocytic pleural effusions. In tuberculous pleurisy, especially, T-helper type 1 (Th1) cytokines are dominant, containing, for example, high concentrations of interferon (IFN)-gamma. We focused on cytokines that induce expression of IFN-gamma and Th1 cell-specific CXC chemokines induced by IFN-gamma. We also evaluated the diagnostic utility of these markers in tuberculous pleural effusions. Forty-three patients with pleural effusions (11 with tuberculous pleuritis, 32 with malignant pleuritis) were studied. We measured the pleural concentrations of IFN-gamma, IFN-gamma-inducing cytokines (interleukin IL-12 and IL-18), and IFN-gamma-inducible chemokines (interferon-gamma-inducible protein of 10-kD [IP-10], monokine induced by interferon-gamma [Mig], and interferon-inducible T-cell alpha chemoattractant [I-TAC]). Our results demonstrate that the concentrations of IFN-gamma, IFN-gamma-inducing cytokines, and IFN-gamma-inducible chemokines were all higher in tuberculous pleural effusions than in malignant pleural effusions. Also, IFN-gamma was significantly correlated with IL-12, Mig, and I-TAC. Moreover, receiver-operator-characteristic (ROC) analysis demonstrated that IFN-gamma produced a greater area under the ROC curve than any other factor. We conclude that the concentrations of IFN-gamma, cytokines that induce expression of IFN-gamma, and chemokines induced by IFN-gamma in tuberculous pleural effusion were all increased. The Th1 chemokines we examined, especially IP-10, are comparable to IFN-gamma as diagnostic markers of tuberculous and malignant pleural effusions, although IFN-gamma is the most valuable.