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Dr. Atul K. Tandon of NeoBiotechnologies discusses the NLRP3/caspase1/IL-18 signaling pathway in the treatment of eosinophilic esophagitis (EoE)

  • Researchers have published new research about eosinophilic esophagitis (EoE), an inflammatory condition primarily affecting children that hinders their ability to eat.
  • Their study reveals that EoE is driven by interleukin-18 (IL-18), an immune system protein, leading to inflammation and the build-up of damaging eosinophils in the esophagus.
  • The research also identifies a potential treatment, VX-765, which selectively targets pathogenic eosinophils without affecting essential white blood cells generated by IL-5.

In a new study  conducted at Tulane University in Louisiana and published in Communications Biology, researchers describe a novel remedy for a persistent inflammatory condition that can make it difficult for children to eat.

Known as eosinophilic esophagitis (EoE), this condition is activated by food allergies or airborne allergens, leading to the accumulation of eosinophils, a specific type of white blood cell, in the esophageal lining.

Consequently, the esophagus becomes shorter and its wall thickens, resulting in difficulties with swallowing and food becoming lodged in the throat.

Detecting symptoms in children can be more challenging and it carries higher risks because feeding difficulties can result in malnutrition and weight loss as well as impacting growth.

Potential to improve the quality of life of children with EoE

Atul Tandon, PhD, the founder, president and chief executive officer of NeoBiotechnologies who was not involved in the research, told Medical News Today that “this paper sheds light on the potential implications of targeting the NLRP3/caspase1/IL-18 signaling pathway in the treatment of eosinophilic esophagitis (EoE).”

“By understanding the mechanisms behind the disease pathogenesis, researchers can develop inhibitors that may protect against the damaging immune response seen in EoE,” he explained.

Source: Medical News Today / See original article here

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