It has long been shown that cells of the nervous system could communicate with cells of the immune system. For instance, the lymphoid organs are innervated by the peripheral nervous system, the sympathetic nervous system, and the parasympathetic nervous system. However, our understanding of local neural pathways that influence immune response at a precise point, lags behind the more explored effect of neurohormonal molecules that are likely to regulate immune responses systemically.
Thus, although it is known that autoimmune diseases can correlate with neurological states like stress, how neural signals are physically transformed into an immune response in the central nervous system is poorly
understood. Using a mouse model of Multiple Sclerosis, experimental autoimmune encephalomyelitis (EAE), Arima and colleagues elegantly showed that autoreactive T cells access the central nervous system via a precise entry door that is located at the fifth lumbar spinal cord. This is controlled by sensory nerve that are activated by the soleus muscle in the leg. Stimulation of the sensory neurons leads to CCL20 expression, a chemokine required for pathogenic CD4 T cell recrutment and accumulation at the fifth lumbar. Interestingly this mechanism is dependent on IL-6 and IL-17.