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Monokine induced by interferon gamma and IFN-γ response to a fusion protein of Mycobacterium tuberculosis ESAT-6 and CFP-10 in Brazilian tuberculosis patients

2005; Elsevier BV; Volume: 8; Issue: 1 Linguagem: Inglês

10.1016/j.micinf.2005.05.019

1769-714X

Clarice Abramo, Krista E. van Meijgaarden, Daniely Garcia, Kees L. M. C. Franken, Michèl R. Klein, Arend J. Kolk, Sérgio C. Oliveira, Tom H. M. Ottenhoff, Henrique Couto Teixeira,

Chemokine receptors and signaling

IFN-γ responses to Mycobacterium tuberculosis antigens ESAT-6 and CFP-10 have been proposed as specific markers of M. tuberculosis infection. Monokine induced by gamma interferon (MIG/CXCL9) has been shown to be expressed by IFN-γ stimulated mononuclear cells and to attract activated T-cells through the chemokine receptor CXCR3. Since MIG is induced early in the response to IFN-γ, measuring MIG may provide an interesting marker to assess downstream IFN-γ induced responses, in contrast to assays that mainly focus on quantifying production of IFN-γ per se. We, therefore, investigated MIG and IFN-γ responses to a fusion protein of ESAT-6 and CFP-10, and compared responses to the conserved mycobacterial antigen 85B (Ag85B) and purified protein derivative (PPD) of M. tuberculosis, in 29 BCG vaccinee controls and 24 TB patients. IFN-γ secreting cells were determined by ELISPOT, and MIG production was measured by ELISA and flow cytometry. Production of MIG in response to ESAT-6/CFP-10, Ag85B and PPD correlated overall with increased numbers of IFN-γ secreting cells (r = 0.55, P < 0.0001). A significant increase was noted among patients compared to controls in the secretion of IFN-γ and MIG following stimulation with ESAT-6/CFP-10 or PPD (P < 0.05). Moreover, MIG intracellular expression was higher in TB patients compared to BCG vaccinees (P < 0.05) in response to ESAT-6/CFP-10 or PPD. We conclude that MIG production correlates significantly with enhanced T-cell IFN-γ production induced by M. tuberculosis-specific antigens ESAT-6/CFP-10. These results point to MIG as a potential novel biomarker that may be helpful in assessing downstream responses induced by IFN-γ in TB.