B-cells with a FasL expressing regulatory phenotype are induced following successful anti-tuberculosis treatment

Immun Inflamm Dis. 2016 Dec 27;5(1):57-67. doi: 10.1002/iid3.140. eCollection 2017 Mar.

Abstract

Introduction: Studies show that B-cells, in addition to producing antibodies and antigen-presentation, are able to produce cytokines as well. These include regulatory cytokines such as IL-10 by regulatory B-cells. Furthermore, a rare regulatory subset of B-cells have the potential to express FasL, which is a death-inducing ligand. This subset of B-cells have a positive role during autoimmune disease, but has not yet been studied during tuberculosis. These FasL-expressing B-cells are induced by bacterial LPS and CpG, thus we hypothesized that this phenotype might be induced during tuberculosis as well.

Methods: B-cells from participants with TB (at diagnosis and during treatment) and controls were collected, and analyzed by means of real-time PCR and flow cytometry. In addition to this, BAL was collected from TB participants as well and analyzed by means of MAGPix (multi-cytokine) technology.

Results: Gene expression analysis show that FASL transcript levels increase by the end of treatment. Similarly, phenotypic analysis show that there is a higher frequency of FasL-expressing B-cells by the end of treatment.

Conclusion: Collectively, these results indicate that these FasL-expressing B-cells are being induced during anti-TB treatment, and thus may play a positive role. Further studies are required to elucidate this.

Keywords: Apoptosis; FasL; broncho‐alveolar lavage fluid; immune exhaustion.

MeSH terms

  • Antitubercular Agents / pharmacology*
  • Antitubercular Agents / therapeutic use
  • B-Lymphocytes / drug effects*
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Bronchoalveolar Lavage Fluid / immunology
  • Cytokines / blood
  • Cytokines / immunology
  • Fas Ligand Protein / genetics*
  • Gene Expression Regulation / drug effects
  • Humans
  • Interleukin-5 Receptor alpha Subunit / genetics
  • Phenotype
  • Tuberculosis, Pulmonary / drug therapy
  • Tuberculosis, Pulmonary / genetics*
  • Tuberculosis, Pulmonary / immunology

Substances

  • Antitubercular Agents
  • Cytokines
  • FASLG protein, human
  • Fas Ligand Protein
  • IL5RA protein, human
  • Interleukin-5 Receptor alpha Subunit