Comparative assessment of regulatory T and B cell phenotype frequencies in active, latent and Tuberculosis negative individuals

Abstract

Background: Literature shows that regulatory B cells (Bregs) and regulatory T cells (Tregs) play a part in the control of many inflammatory diseases including tuberculosis (TB) by regulating the CD4 Tcell responses. This may impact on the outcome of Mycobacteria tuberculosis (Mtb) infection and the differences in the numbers of these cells at the time of Mtb infection may determine the outcome of TB infection status. However, Bregs or and Tregs phenotypes have been understudied, with the few studies done so far yielding conflicting results. Further still these studies were carried out in low TB endemic areas. Methods: This study analyzed and compared frequencies of Treg and Breg phenotypes in active TB (ATB) individuals and their latently infected and noninfected house hold contacts (HHC) in a high TB endemic area. Cryopreserved peripheral blood mononuclear Cells (PBMC) were thawed, washed and stained using fluorochrome-labelled antibodies for reported Treg and Breg markers and analysed using flow cytometry. Results: Individuals with ATB had lower frequencies of Bregs compared to the non infected and Latent TB infected (LTBI) HHC. Non infected HHC had elevated frequencies of transitional Bregs(CD24hiCD38hi) compared to both active TB and LTBI. We did not observe any differences in Classical Bregs (CD1d+), Memory Bregs (CD24hiCD27+), and plasma blasts(CD27+CD38hi) between any of the groups. Tregs phenotypes were not different between the groups and there was no correlation between frequencies of Bregs and Tregs. Conclusion: The regulatory T and B cell immune cells in latent and ATB infection are similar in distribution butare higher in uninfected TB state. This indicates that Mtb induces an immune regulatory state as anticipated, however the TB status does not influence the extent of response and differences in frequencies of the assesed Bregs and Tregs phenotypes may not distinguish between active and latent TB states.