A recent study in mice shows immunological differences that separate people who experience significant itching from insect bites from those who do not. (Image credit: dorioconnell via Getty Images)
Some people can't help but itch after a mosquito bite — but not everyone itches after an insect bite or other allergen. Now, a new study in mice reveals differences in immune system function that may determine whether you end up scratching.
The skin is filled with sensory neurons, which are nerve cells that detect changes in the environment and cause sensations such as pain. When a person encounters a potential allergen, such as mosquito saliva, these neurons detect it and can initiate an itchy response. They also help activate nearby immune cells, which trigger an inflammatory response that causes swelling and redness.
Some people who are repeatedly exposed to an allergen may develop chronic allergic inflammation, which fundamentally changes the tissues where the inflammation occurs. For example, immune cells that respond to allergens may change the sensitivity of nerves, making them more or less likely to react to the substance.
“We all have sensory neurons, so we can all feel itchy — but not all of us develop allergies, even though we’re surrounded by the same allergens,” senior study author Dr. Caroline Sokol, a professor of allergy and immunology at Harvard Medical School and Massachusetts General Hospital, told Live Science. “So what determines whose sensory neurons fire in response to allergens and whose don’t?”
To find out, Sokol and her team exposed mice to a chemical called papain, which produces an itchy sensation, causing the mice to scratch their skin. Different groups of lab mice in the study were missing different immune cells. The study, published Wednesday (Sept. 4) in the journal Nature, found that mice missing a certain type of T cell did not scratch when exposed to papain.
The researchers wanted to find out how these cells, called GD3 cells, affect sensory nerve responses. They grew GD3 cells in the lab and treated them with a chemical to make them release signaling molecules known as cytokines. They then injected mice with normal immune systems with fluid containing the cytokine in which the cells had been grown.
The treatment itself did not cause itching. However, it increased the mice's scratching responses to various allergens, including mosquito saliva. This suggests that something secreted by the GD3 cells was increasing the itch caused by the nerves.
By comparing the chemicals secreted by GD3 cells with those of other immune cells in the skin's central layer, the researchers found that only one factor was unique to GD3 cells: interleukin 3 (IL-3), which is known to help regulate inflammation.
Only some sensory neurons responded to IL-3. Those that did became more likely to itch, a sign that the cytokine was “priming” neurons to respond to allergens.
In contrast, when the researchers knocked out the genes for IL-3 or its receptors — or removed the GD3 cells entirely — the mice were unable to initiate an allergic reaction. In additional experiments, the researchers concluded that IL-3 activates two separate signals: one that promotes nerve-induced itch and one that controls the immune side of the allergic reaction.
By releasing IL-3, the GD3 cells were “absolutely essential” for setting the threshold at which sensory nerves would respond to the allergen, Sokol said. This chain reaction involving IL-3 “may give us a new avenue for treating patients with chronic itch disorders,” she added.
However, the study has only been conducted on mice so far, so scientists cannot be sure that human cells will respond in the same way. Although the mouse immune cells in the study have very similar genes and proteins to their human counterparts, Sokol emphasized
Sourse: www.livescience.com
