The skin is abundant sensory (sensory) neuronsthat is, nerve cells that detect changes in the environment and, in response to them, cause sensations – for example, pain. When a person encounters a potential allergen – for example, mosquito saliva – these neurons detect it and can cause an itchy sensation. They are too helps activate nearby immune cellswhich cause an inflammatory reaction manifested by swelling and redness.
For some people who are repeatedly exposed to an allergen, chronic allergic inflammation may developwhich essentially changes the tissues in which that inflammation occurs. For example, immune cells responding to allergens can change the sensitivity of nerves, making them more or less responsive to the substance.
“We all have sensory neurons, so we can all feel itch, but not everyone is allergic, even though we are surrounded by the same allergens,” says senior author of the study, Dr. Caroline Sokol, professor of allergy and immunology at Harvard Medical School and Massachusetts General Hospital (USA). “So what determines whose sensory neurons respond to allergens and whose do not?”
To find out, Sokol and his colleagues exposed mice to a chemical called papain, which causes an itch that causes the mice to scratch their skin. Different groups of lab mice in the study lacked different immune cells. In a study published in the journal Nature found that mice lacking a certain type of T cell did not dig – when exposed to papain.
The researchers wanted to find out how these cells, called GD3 cells, stimulated sensory nerve responses. They grew GD3 cells in the lab and treated them with a chemical to make them release signaling molecules called cytokines. They then injected mice with normal immune systems with a fluid containing cultured cells and containing cytokines.
It didn’t itch by itself. However, it increased scratching in mice in response to various allergens, including mosquito bites. This suggested that something secreted by GD3 cells enhanced nerve-mediated itch.
After comparing the chemicals released by GD3 cells to those released by other immune cells in the middle layer of the skin, the researchers found that only one factor was unique to GD3 cells: interleukin 3 (IL-3), which is known to helps regulate inflammation.
Only some sensory neurons responded to IL-3. Those that responded were more likely to itch, a sign that the cytokine is “priming” neurons to respond to allergens.
In contrast, when the researchers deleted the genes for IL-3 or its receptor, or completely removed the GD3 cells, the mice were unable to experience an allergic reaction. After further experiments, the researchers concluded that IL-3 activates two separate signals: one that promotes nerve-mediated itch and another that controls the immune side of the allergic reaction.
By secreting IL-3, GD3 cells were “absolutely essential” in setting the threshold at which a sensory nerve responds to an allergen, Sokol said. This chain reaction involving IL-3 “may give us a new way to treat patients with chronic itch disorders,” she added.
But so far, the research has only been done on mice, so scientists can’t be sure that human cells will behave in exactly the same way. Although the immune cells in the mice involved in the study have very similar genes and proteins to their human counterparts, the researcher emphasized that it is important to understand whether and how human T cells respond to IL-3. These data are needed to translate the discovery into treatments for itching or ways to predict who might be at risk for allergies.
“We all have a friend who doesn’t react to mosquito bites and a friend who looks terrible after a day outside,” says Sokol. – We think so [IL-3] this is determined in real time, because when we look at the itch caused by mosquito bites – and the allergic immune response that follows – we see that it is completely dependent on the cells in this pathway.”
Parengta pagal „Live Science“.
2024-09-05 20:47:24