Notably, GM-CSF-deficient mice are resistant to EAE.47 Emerging evidence suggests that GM-CSF is involved in autoimmune diseases.48 In MS, GM-CSF has been suggested to define a T-helper cell signature.49 In support of our findings that the lack of Adam12 results in fewer Th1 cells that express GM-CSF while failing to influence Th17 cells, it has been reported that in human T cells, IL-17 and GM-CSF expression is antagonistically regulated by human T-helper cells, wherein GM-CSF is associated with the Th1 axis.50 This evidence concerns the gene IL17A and myeloid sarcoma.