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

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)-γ. We focused on cytokines that induced expression of IFN-γ and Th1 cell–specific CXC chemokines induced by IFN-γ. 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-γ, IFN-γ–inducing cytokines (interleukin [IL]-12 and IL-18), and IFN-γ–inducible chemokines (interferon-gamma-inducible protein of 10-kD [IP-10], monokine induced by interferon-gamma [Mig], and interferon-inducible T-cell α chemoattractant [I-TAC]). Our results demonstrate that the concentrations of IFN-γ, IFN-γ–inducing cytokines, and IFN-γ–inducible chemokines were all higher in tuberculous pleural effusions than in malignant pleural effusions. Also, IFN-γ was significantly correlated with IL-12, Mig, and I-TAC. Moreover, receiver-operator–characteristic (ROC) analysis demonstrated that IFN-γ produced a greater area under the ROC curve than any other factor. We conclude that the concentrations of IFN-γ, cytokines that induced expression of IFN-γ, and chemokines induced by IFN-γ in tuberculous pleural effusion were all increased. The Th1 chemokines we examined, especially IP-10, are comparable to IFN-γ as diagnostic markers of tuberculous and malignant pleural effusions, although IFN-γ is the most valuable. 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)-γ. We focused on cytokines that induced expression of IFN-γ and Th1 cell–specific CXC chemokines induced by IFN-γ. 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-γ, IFN-γ–inducing cytokines (interleukin [IL]-12 and IL-18), and IFN-γ–inducible chemokines (interferon-gamma-inducible protein of 10-kD [IP-10], monokine induced by interferon-gamma [Mig], and interferon-inducible T-cell α chemoattractant [I-TAC]). Our results demonstrate that the concentrations of IFN-γ, IFN-γ–inducing cytokines, and IFN-γ–inducible chemokines were all higher in tuberculous pleural effusions than in malignant pleural effusions. Also, IFN-γ was significantly correlated with IL-12, Mig, and I-TAC. Moreover, receiver-operator–characteristic (ROC) analysis demonstrated that IFN-γ produced a greater area under the ROC curve than any other factor. We conclude that the concentrations of IFN-γ, cytokines that induced expression of IFN-γ, and chemokines induced by IFN-γ in tuberculous pleural effusion were all increased. The Th1 chemokines we examined, especially IP-10, are comparable to IFN-γ as diagnostic markers of tuberculous and malignant pleural effusions, although IFN-γ is the most valuable.