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Neuronal-ILC2 Interactions: A New Frontier in Regulating Glucose Homeostasis

By Aarav Shah,

The Lawrenceville School, NJ


Research involving connections between both the neural system and immune system has taken great strides, most recently involving the relationship between type 2 innate lymphoid cells (ILC2) and the homeostasis of blood sugar levels. Through conducting a study involving mice, scientists and researchers explored, tested, and ultimately noticed a trend regarding the importance of ILC2, “...a rare type of immune cell,” and the secretion of glucagon.1-3 Post sixteen-hour periods of fasting, mice that had a paucity of ILC2s did not have an effective release of glucagon, and thus blood sugar homeostasis levels did not efficiently restore back to normal.1,2


Image from Science.org 
Image from Science.org 

Further investigation and experiments supports the notion that, normally, organisms with sufficient amounts of ILC2s allow for an intricate cycle to take place, ultimately bringing the blood glucose levels back to normal.1,2 This repetitive cycle begins with the stimulus, a lack of glucose, or sugar, in the bloodstream.1,2 This is promptly followed by adrenergic neuronal signals, which essentially break free the ILC2s from their “...gut-anchoring receptors.”1,2 From this point, the ILC2s travel to the pancreas, where some have been found inside the islets of Langerhans, the location from which glucagon begins its process in entering the bloodstream (via the help of alpha cells).2 There, it has been discovered that the ILC2s help provoke the alpha cells to secrete glucagon, a hormone that assists with “gluconeogenesis and endogenous glucose production in the liver.”1,2 With an increase in the generation of glucagon, glycogen and noncarbohydrate substrates ultimately convert into the form known as endogenous glucose.2 This helps increase the blood sugar, bringing the blood glucose levels back to normal levels, or the state of homeostasis.1,2 


Because of these scientific breakthroughs, now comes the possibility for novel and effective treatment therapies. Among these remedies include treatments for hypoglycemia, an illness by which those affected have abnormally low blood sugar levels.4 The standard fasting blood sugar is approximately 70 mg/dL (milligrams/deciliter).4 Starting with shakiness and fatigue, hypoglycemia can eventually lead to imbalance or slurred speech.4 From a scientific perspective, the loss of coordination and tiredness can arise because with a lack of sugar, cellular respiration cannot be performed. Cellular respiration is crucial for the production of ATP, a usable form of energy for cells around the body. Thus, without this energy, it is easy to have a lack of motivation and/or strength to perform a physical activity. Anyhow, the neuronal-ILC2 interaction discovery would allow medical professionals and scientists to see how these immune cells could potentially assist with more glucagon secretion.2,3 In other words, if the goal is to raise blood sugar levels back to normal, one way to do that could be understanding how to use neuron signals to spur ILC2s to migrate to the pancreas – this would eventually lead to that increase in blood glucose.1,2


Moving forward, the medical industry has the opportunity to understand the risk/benefit assessment of using neuron signals and ILC2s to stimulate the release of glucagon.2 Targeted treatment options for low blood glucose could become an option, as neuronal signals are responsible for allowing ILC2s to migrate to the pancreas.1,2


----Works Cited

Šestan, M., et al. (2025). Neuronal-ILC2 interactions regulate pancreatic glucagon and glucose homeostasis. Science, 387(6731), eadi3624. https://doi.org/10.1126/science.adi3624


Science. (2025). Neuronal-ILC2 interactions regulate pancreatic glucagon and glucose homeostasis. https://www.science.org/doi/10.1126/science.adi3624



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