Amoeboid movement in human leucocytes: basic mechanisms, cytobiological and clinical significance.
The present paper is an analytical review of the information available on amoeboid movement in human leucocytes. The reported evidence suggests that leucocyte locomotion is due to pressure developed in the cell cortex in the middle and posterior parts of the moving cell, that 4 nm fibrils may provide at least part of the ultrastructural basis of locomotion, that actin-like and myosin-like proteins may be involved in the mechanism of movement and that ATP may serve as an energy source. Leucocyte motility appears to be governed mainly by factors produced in the external medium. Neutrophil chemotaxis is the most antitubulin-susceptible cell mechanism known; from this observation an essential role of microtubule redistribution in chemotaxis is inferred. In contrast, the random movement of neutrophils is not appreciably affected by antimitotic concentrations of antitubulins. Amoeboid movement seems to be an important mechanism in the short-distance locomotion and immunological functions of leucocytes.
D000199:Actins / Q000502:physiology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002449:Cell Aggregation; D002465:Cell Movement; D002634:Chemotaxis, Leukocyte; D006098:Granulocytes / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007962:Leukocytes / Q000502:physiology*; D008198:Lymph Nodes; D008214:Lymphocytes / Q000502:physiology; D008870:Microtubules / Q000502:physiology; D009000:Monocytes / Q000502:physiology; D009218:Myosins / Q000502:physiology; D009504:Neutrophils / Q000502:physiology
D000199:Actins; D000255:Adenosine Triphosphate; D009218:Myosins