Earlier studies found no evidence of abnormal blood levels of interleukin 5, interleukin 3, or granulocyte-macrophage colony stimulating factor. A more recent study used a more sensitive assay for interleukin 5 to compare members of a single extended family with some members lacking the disorder. The study found that members with the disorder had: a) peripheral blood mononuclear cells as well as T helper cells (major physiological source of interleukin 5), CD8+ cells, CD14+ cells, and CD19+ cells that expressed high levels of messenger RNA for interleukin 5 while their peripheral blood mononuclear cells expressed normal levels of messenger RNA for RAD50, a gene in close proximity to IL-5; b) elevated serum levels of interleukin 5 as well as soluble Interleukin 5 receptor alpha subunit; and c) innate lymphoid cells (also major physiological sources of interleukin 5) that produced increased amounts of interleukin 5 in response to stimulation. A second family with asymptomatic eosinophilia over three generations likewise exhibited increased production of interleukin 5. These studies suggest that the dis-regulated overproduction of interleukin 5 by blood mononuclear cells is an underlying cause of the eosinophilia found in at least some families with this disorder.
Familial eosinophilia
Tropical eosinophilia
Hypereosinophilic syndrome
Hereditary angioedema
Lymphocyte-variant hypereosinophilia
Mast cell activation syndrome
Drug reaction with eosinophilia and systemic symptoms
Mixed connective tissue disease