In a study published in the research journal Scientific Reports, CD71+ erythroid cells (CECs) have an immunoregulatory function. They often appear in people with cardiopulmonary or hemolytic disorders, as well as in newborns. The goal of this study was to investigate the activity of CECs in response to systemic inflammation, such as that which occurs in systemic-onset juvenile idiopathic arthritis.
About Juvenile Idiopathic Arthritis
Juvenile idiopathic arthritis is a rare form of arthritis that primarily affects children and teens. While it is known that the disease is autoimmune in origin (meaning that the immune system begins to attack healthy tissue by mistake), what triggers the beginning of the autoimmune response is not known. Any disease considered “idiopathic” does not have an identified cause. Some risk factors for juvenile idiopathic arthritis include being female and a family history of the disease. Symptoms include limping, vague flu-like symptoms, fatigue, loss of appetite, swelling of the joints, joint pain and stiffness, growth problems, and eye inflammation. The disease can also lead to complications such as vision problems, osteoporosis, joint deformities, and contractures. Treatment approaches often include physical therapy, NSAIDs, corticosteroids, and certain chemotherapy agents that suppress the immune system. Surgery may be necessary in severe cases. To learn more about juvenile idiopathic arthritis, click here.
About The Research
The scientists recognized that the peripheral blood mononuclear cells of these patients upregulated the genes related to erythropoiesis. In this study, the most prominent upregulated gene was ARG2. In comparison to other inflammatory illnesses, the expansion of CECs appeared the largest in systemic onset juvenile idiopathic arthritis.
In the erythropoiesis process, hepcidin and erythropoietin have opposing roles; however, the scientists found that their serum levels were in sync with levels of circulating CECs. In addition, CECs were also correlated with the levels of soluble TNF receptors, C-reactive protein, IL-18, and IL-6. When compared to other inflammatory illnesses, the CECs move to the periphery during the most acute phase of this disease to a greater extent.
The scientists theorize that circulating CECs control regulate excess inflammation, a process that may partially involve arginase-2.