#Sociability

New research from MIT and Harvard Medical School shows that cytokines—immune molecules that battle infections—also influence brain function and behavior. The findings suggest that illness can alter mood and social interactions not only through fatigue but via direct immune-brain connections. This could help explain aspects of conditions such as autism and depression.

Among the cytokines studied, IL-17 appears to have region-specific effects in the brain. In the amygdala, IL-17 heightens anxiety, while in the somatosensory cortex it seems to increase sociability. The results highlight a complex dialogue between the immune system and neural circuits, pointing to new avenues for understanding how immune activity shapes behavior during illness.

Recent cutting-edge research from MIT and Harvard Medical School reveals that cytokines, immune molecules that play a crucial role in fighting infections, also affect brain functions, inducing profound behavioral changes such as anxiety or increased sociability. This discovery opens new avenues for understanding the interconnectedness of the immune and nervous systems and illuminates potential pathways for treating neurological conditions like autism and depression.

Cytokines, including a variety named IL-17, have been the focus of these transformative studies. Researchers discovered that IL-17 operates in the brain’s distinct regions—the amygdala and the somatosensory cortex—eliciting contrasting effects. Within the amygdala, IL-17 induces anxiety, while in the cortex, it promotes sociability. These dual roles underscore a complex interaction between the brain and immune system, suggesting that behavioral changes during illness are not solely due to physical fatigue but also to brain functions being directly modulated by immune activity.