Researchers from MIT and Harvard Medical School have uncovered compelling evidence linking infection-fighting molecules, specifically cytokines, to behavioral and mood shifts during illness. This work expands the conventional view of cytokines, highlighting their influence beyond immunity and into the realm of neurology. By mapping cytokine receptor locations in the brain, especially for forms of IL-17, the team discovered these molecules can directly modulate behaviors associated with sickness.
The scientists found that IL-17 targets distinct brain regions to produce varying effects. In the somatosensory cortex, the cytokine seems to promote sociable behavior by interacting with a specific set of neurons. Intriguingly, these neurons are tied to autism-like symptoms in mice, and the presence of IL-17 appears to make them less excitable. This reduction in neuronal activity may explain clinical observations, such as the temporary alleviation of autism symptoms in children during bouts of fever, potentially due to increased IL-17 levels. One hypothesis presented by senior author Gloria Choi posits that IL-17 may have first evolved as a neuromodulator, only later being adapted by the immune system for pathogen defense.
The study also highlighted a connection between IL-17 and increased anxiety, mediated through receptors found in neurons within the amygdala—a region essential for emotion processing. Here, IL-17 binding leads to heightened neuron excitability and subsequent anxiety responses. Altogether, these findings present a significant advance in neuroscience and immunology, reinforcing the deep interconnection of the immune and nervous systems. Looking forward, this research could pave the way for novel therapies targeting immune-neural interactions in conditions like autism and depression.
