Research shows a surprising connection between pain-sensing neurons and immune cells, which may help us understand immune processes and be a target for treatments.
, however, noted that in some patients, nerve damage in one limb caused them to lose sensation and psoriasis in that limb. As the nerves regenerated and sensation returned, though, so did the psoriasis.How the neurons are communicating with the immune cells, however, remained a mystery. Until now.Dendritic cells are the “guardians” of our immune system.
This signal also acts as a “stay here” cue, which gives dendritic cells time to gather intel about pathogen threats. When dendritic cells detect antigens from a pathogen , they rush off to the lymph nodes to activate the rest of the immune system. Dendritic cells then load themselves with inflammatory cytokines for a more potent effect, but this does not cause inflammation by itself. Instead, it waits for a “go” signal.
These studies were conducted with mice because there are limits to the kinds of experiments we can feasibly and ethically perform in humans. While we don’t know whether the same processes occur in humans, the cell types and molecules involved are evolutionarily conserved and thought to function similarly in our bodies, the researchers said.“I really anticipate that this would translate pretty well into humans,” said Talbot, who was not involved in the study.
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