Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Jul:111:145-151.
doi: 10.1016/j.molimm.2019.04.012. Epub 2019 May 1.

Bcells and their regulatory functions during Tuberculosis: Latency and active disease

Affiliations
Free article
Review

Bcells and their regulatory functions during Tuberculosis: Latency and active disease

Andre G Loxton. Mol Immunol. 2019 Jul.
Free article

Abstract

Tuberculosis (TB) is a global epidemic with devastating consequences. Emerging evidence suggests that B-cells have the ability to modulate the immune response and understanding these roles during Mycobacterium tuberculosis (M.tb) infection can help to find new strategies to treat TB. The immune system of individuals with pulmonary TB form granulomas in the lung which controls the infection by inhibiting the M.tb growth and acts as a physical barrier. Thereafter, surviving M.tb become dormant and in most cases the host's immunity prevents TB reactivation. B-cells execute several immunological functions and are regarded as protective regulators of immune responses by antibody and cytokine production, as well as presenting antigen. Some of these B-cells, or regulatory B-cells, have been shown to express death-inducing ligands, such as Fas ligand (FasL). This expression and binding to the Fas receptor leads to apoptosis, a major immune regulation mechanism, in addition to the ability to induce T-cell tolerance. Here, I discuss the relevance of B-cells, in particular their non-humoral functions by addressing their regulatory properties during M.tb infection.

Keywords: Apoptosis; B-cells; FasL; Latency; Non-humoral; Regulatory B-cells; Tuberculosis.

PubMed Disclaimer

Publication types

MeSH terms