Populations of two phenotypes of CD4+ T cells, ThCD103 (a TNFα secreting population), and ThGM, which produce granulocyte–monocyte colony-stimulating factor (GM-CSF) and are pro-inflammatory [128], were found to be sequestered in the thymus and reduced in the peripheral circulation of MG patients, the latter correlating inversely with disease severity [129]. Here, CSF2 is linked to myasthenia gravis.