Research Fellows Directory
Dr Diego Catalan
University College London
B cells are a key part of the immune system, defending the body against invading pathogens. In contrast, regulatory B cells (Bregs) are a type of B cell that protect against excessive inflammation. They do so by releasing a chemical mediator, called interleukin-10, that restrains potentially harmful cells. In this way, Bregs can prevent the development and progression of autoimmune diseases, and may play a role in the resolution of protective immune responses.
Recently, we have made two important findings. Firstly, that the commensal bacteria in the gut contribute to both the development of inflammation in mice and the differentiation of Bregs. Currently, it is unclear which bacteria instruct B cells to become protective or harmful. Secondly, we have data showing that mice with arthritis have leaky guts. A leaky gut is when the lining of the digestive tract is damaged and fails to work as a barrier that keeps out bigger particles or microorganisms that can damage the organism. The presence of a leaky gut could allow some bacteria or their components to cross the intestinal lining and cause the activation of the immune system, leading to the development, or worsening, of inflammatory diseases. In agreement with this idea, we have also observed that mice with arthritis benefit from a treatment that reduces gut permeability.
Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease, where the patient’s immune system attacks the body’s own organs, such as the kidneys and the central nervous system. In SLE patients, Bregs don't work properly, and their malfunctioning may contribute to disease. We are now studying patients with SLE in order to establish whether they have increased gut permeability compared to healthy controls, whether the gut commensal bacteria or their metabolic products differ between SLE patients and healthy individuals, and how these variations correlate with Bregs number and function, and with the severity of disease.