title: B-cells with a FasL expressing regulatory phenotype are induced following successful anti-tuberculosis treatment.
abstract: 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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Division of Molecular Biology and Human Genetics Faculty of Medicine and Health Sciences SA MRC Centre for TB Research DST/NRF Centre of Excellence for Biomedical Tuberculosis Research Stellenbosch University Cape Town South Africa.
authors.forename: Ilana C
authors.initials: IC
authors.lastname: van Rensburg
authors.affiliation: Division of Molecular Biology and Human Genetics Faculty of Medicine and Health Sciences SA MRC Centre for TB Research DST/NRF Centre of Excellence for Biomedical Tuberculosis Research Stellenbosch University Cape Town South Africa.
authors.forename: Léanie
authors.initials: L
authors.lastname: Kleynhans
authors.affiliation: Clinical Laboratory Sciences Faculty of Health Sciences University of Cape Town Cape Town South Africa.
authors.forename: Alana
authors.initials: A
authors.lastname: Keyser
authors.affiliation: Division of Molecular Biology and Human Genetics Faculty of Medicine and Health Sciences SA MRC Centre for TB Research DST/NRF Centre of Excellence for Biomedical Tuberculosis Research Stellenbosch University Cape Town South Africa.
authors.forename: Gerhard
authors.initials: G
authors.lastname: Walzl
authors.affiliation: Division of Molecular Biology and Human Genetics Faculty of Medicine and Health Sciences SA MRC Centre for TB Research DST/NRF Centre of Excellence for Biomedical Tuberculosis Research Stellenbosch University Cape Town South Africa.
authors.forename: Andre G
authors.initials: AG
authors.lastname: Loxton
mesh_terms: D000995:Antitubercular Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016207:Cytokines / Q000097:blood / Q000276:immunology; D053222:Fas Ligand Protein / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D053666:Interleukin-5 Receptor alpha Subunit / Q000235:genetics; D010641:Phenotype; D014397:Tuberculosis, Pulmonary / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology
chemical_list: D000995:Antitubercular Agents; D016207:Cytokines; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C485918:IL5RA protein, human; D053666:Interleukin-5 Receptor alpha Subunit
keywords: Apoptosis; FasL; broncho‐alveolar lavage fluid; immune exhaustion