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The immune characterization of interferon-β responses in tuberculosis patients

Xiao Zhang1, Yi Sun2, Caiyun He1

  • 1State Key Laboratory of Oncology in South China, Department of Molecular Diagnostics, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.

Microbiology and Immunology
|March 6, 2018
PubMed

Insights

Tuberculosis pleurisy involves spontaneous expression of IFN-β, IL-17, and IFN-γ in pleural fluid cells. Interferon-beta (IFN-β) suppresses IL-17 while boosting IFN-γ, suggesting caution in IFN-β targeted tuberculosis treatments.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Respiratory Medicine

Background:

  • Tuberculous pleurisy is an inflammatory condition affecting the pleural space.
  • The roles of key cytokines like Interferon-beta (IFN-β), Interferon-gamma (IFN-γ), and Interleukin-17 (IL-17) in tuberculous pleurisy are not fully understood.
  • Understanding immune responses is crucial for developing effective anti-tuberculosis strategies.

Purpose of the Study:

  • To investigate the immunoregulatory effects of IFN-β in patients with tuberculous pleurisy.
  • To analyze the expression levels and correlations of IFN-β, IFN-γ, and IL-17 in pleural fluid.
  • To determine the impact of IFN-β on IL-17 and IFN-γ production in this context.

Main Methods:

  • Detection of IFN-β, IFN-γ, and IL-17 expression in pleural fluid mononuclear cells (PFMC) from tuberculous effusions and peripheral blood mononuclear cells (PBMC) from healthy donors.
  • Analysis of cytokine expression following exogenous IFN-β stimulation of PFMC.
  • Assessment of cytokine regulation using IFN-β and IFN-γ neutralizing antibodies in bacillus Calmette-Guérin (BCG)-stimulated PFMC.

Main Results:

  • Freshly isolated PFMC from tuberculous pleurisy spontaneously expressed IFN-β, IL-17, and IFN-γ, unlike PBMC from healthy individuals.
  • Exogenous IFN-β inhibited IL-17 expression but enhanced IFN-γ production in PFMC.
  • Neutralization of endogenous IFN-β led to increased IL-17 and decreased IFN-γ, while IFN-γ neutralization increased IL-17 production.

Conclusions:

  • IFN-β plays a significant immunoregulatory role in tuberculous pleurisy, suppressing IL-17 and promoting IFN-γ.
  • Both IFN-β and IFN-γ contribute to the down-regulation of IL-17.
  • These findings highlight the complex interplay of cytokines and suggest caution is needed when considering IFN-β inhibition as an anti-tuberculosis therapeutic approach.

Keywords:
IFN-βbacillus Calmette-Guérin (BCG)pleural fluid mononuclear cell (PFMC)

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