Rescuing Regulatory B cells Function May Be A New Therapeutics Strategy for Systemic Sclerosis

Rescuing Regulatory B cells Function May Be A New Therapeutics Strategy for Systemic Sclerosis

In a recent study entitled “B regulatory cells are decreased and functionally impaired in patients with systemic sclerosis”, researchers report that a specific population of B cells – regulatory B cells – with established functions in immune suppression, have their numbers markedly reduced and functions impaired in systemic sclerosis patients. These findings suggest a potential new therapeutics for systemic sclerosis patients by rescuing regulatory B cells function. The study was published in the Arthritis & Rheumatology journal.

Systemic sclerosis, also known as scleroderma (meaning hard skin), is characterized by excessive deposition of collagen in the skin, although the disease frequently progresses into a systemic disease therefore affecting internal organs, such as kidneys, heart, lungs and intestine. The disease induces vascular damage, fibrosis and autoantibodies production. Scleroderma remains a disease with high mortality and no effective treatment.

Immune cells, such as T cells, have been implicated in systemic sclerosis disease pathogenesis, but the role of B cells (immune cells responsible for antibody production) remains largely unknown, despite the fact that B cell infiltrates can be observed in systemic sclerosis lesions. Recently, a small population of B cells named regulatory B cells (Bregs) was reported to modulate and suppress immune responses, thereby preventing autoimmunity. This was achieved by secreting interleukin 10 (IL-10).

The authors determined the number and function of Bregs in systemic sclerosis, particularly the Bregs-producing IL-10. To this end, the team measured Bregs in 45 patients with systemic sclerosis (from which 12 patients had early disease and 33 had systemic sclerosis-associated pulmonary fibrosis), 10 healthy controls and 10 patients with rheumatoid arthritis-associated pulmonary fibrosis. They found that not only Bregs numbers were decreased in systemic sclerosis patients, but were also functionally impaired as their expression of IL-10 was significantly reduced upon Bregs stimulation.

B10 cells (IL-10 producing) negatively regulate inflammation and autoimmunity, with studies in mice showing B10 cells ameliorate collagen-induced arthritis. These findings suggest that the decreased number of Bregs and inability to produce IL-10 after stimuli have implications in systemic sclerosis pathogenesis. Hence, ex vivo expansion of B10 cells and their administration back into systemic sclerosis patients may constitute a potential new treatment strategy for systemic sclerosis.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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