Defective polymorphonuclear chemotaxis in patients with Turner's syndrome (45,X).

Polymorphonuclear leucocytes from patients with full Turner's syndrome (45,X) revealed a significantly weaker chemotactic response towards zymosan-activated serum than normal female and male controls. Random mobility and chemokinetic responses of polymorphonuclear leucocytes were normal, and so were all locomotive responses of mononuclear phagocytes in patients with Turner's syndrome. A subclinical polymorphonuclear leucocyte chemotactic defect is suggested by these results, and a possible regulatory effect by a gene(s) in chromosome X (and Y) that must be present in a full double dose to preserve this function can be proposed. Control of polymorphonuclear leucocyte chemotaxis may represent yet another exception to the general rule of X-inactivation.