Crohn's disease (CD) is a chronic illness that affects about 2.5 million people all over the world. A cytokine named Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) in the human body can maintain the immune balance of the intestinal tract so that the intestinal tract can maintain normal physiological function. However, anti-GM-CSF autoantibodies (aGMAb) were found in the blood of CD patients, and the presence of this antibody could prevent GM-CSF from functioning properly.
In a recently published paper in Gastroenterology, scientists analyzed blood samples from soldiers with CD at a biologic repository run by the U.S. military during their enlistment and after their illness. At the same time, blood samples from healthy people and patients with ulcerative colitis were also included in the analysis, which helped them to find out the detailed mechanism of aGMAb. According to their research, GM-CSF can be neutralized by the aGMAb and lead to the destruction of the immune system. Over a long period, the lower part of the small intestine can be severely damaged, which can lead to CD. In addition, the aGMAb can be detected long before disease occurs, so this finding may have important implications for early intervention in CD.
It is worth noting that aGMAb is not present in all CD patients, and the severity and form of patients with aGMAb are different.
Mortha and coworkers have established a team to figure out the recognized region site of GM-CSF and further try to modify GM-CSF to prevent it from being neutralized by aGMAb to treat the disease. Overall, the discovery of aGMAb in patients with CD and its pathogenesis makes it a potential serum biomarker for the diagnosis of potential patients. At the same time, the targeted modification of GM-CSF to prevent its specific binding to aGMAb also provides an effective idea for the treatment of complicated CD.
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