Modulating monocytes could benefit ALS

Aberrant immune responses are probably involved in the pathogenesis of amyotrophic lateral sclerosis (ALS). This paper studied the role of innate immunity in a mouse model of ALS. During disease progression, inflammatory monocytes — the LY6C^hi subset — were recruited via chemokine receptor 2 to the spinal cord (but not the brain), and this correlated with neuronal loss. Treatment of mice with an LY6C-specific antibody reduced neuronal loss and increased survival. Moreover, analogous monocytes from patients with ALS had a similar inflammatory phenotype to monocytes from the mouse model.