Effect of binding immunoglobulin protein on induction of regulatory B cells with killer phenotype during inflammation and disease
Date
2019-03-05
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Future Science
Abstract
Immune responses result from different immune cells acting in synergy to successfully fight infections.
This requires a high degree of regulation to prevent excessive production of inflammatory products leading
to other disease forms. Regulatory B cells are classified based on surface immunoglobulin expression.
These cells are reported to resolve inflammation during chronic or autoimmune diseases. However, during
chronic inflammation, their frequencies have been shown to be affected, and they can be induced
by exposure to extracellular binding immunoglobulin protein (BiP). This review focuses on the effects on
immune cells by extracellular or secreted BiP during various chronic inflammatory responses. For example,
cell stress associated with Mycobacterium tuberculosis infection leads to accumulation of unfolded proteins
that subsequently activate BiP and its three signal transducers intracellularly. Furthermore, BiP can
be translocated from the endoplasmic reticulum to the extracellular environment where it binds immune
cells as an autoantigen and leads to functional changes.
Description
CITATION: Motaung, B. & Loxton, A. G. 2019. Effect of binding immunoglobulin protein on induction of regulatory B cells with killer phenotype during inflammation and disease. Future Science OA, 5(3):FSO379, doi:10.4155/fsoa-2018-0121.
The original publication is available at https://www.future-science.com
The original publication is available at https://www.future-science.com
Keywords
Apoptosis, Autoimmune diseases, Immunoglobulin-binding proteins -- Bacterial, Chronic diseases, Immune response, Mycobacterium tuberculosis -- Infections, Necrosis, Inflammation, B cells, B Lymphocytes
Citation
Motaung, B. & Loxton, A. G. 2019. Effect of binding immunoglobulin protein on induction of regulatory B cells with killer phenotype during inflammation and disease. Future Science OA, 5(3):FSO379, doi:10.4155/fsoa-2018-0121.