The cytoskeleton in activated and in functionally disordered cells of the macrophage system

In animal experiments, and for various granulomatous diseases of humans, components of the so-called cytoskeleton in cells of the macrophage system were investigated in the electron microscope and with the aid of indirect immunofluorescence microscopy using monospecific antibodies. In young monocytes and in non-activated or only slightly activated mononuclear phagocytes, predilection areas and characteristic patterns of arrangement were found: F-actin is observable, densely arranged, in particular, around the nucleus and below the cytomembrane; intermediate filaments of the vimentin type form a broad, intensely fluorescent wreath around the cell nucleus; microtubules radiate from the perinuclear centriole in all directions into the neighbouring cytoplasm, taking the form of a microaster. Modifications of this pattern of distribution begin in the pre-mitotic phase, and become highly evident in karyokinesis and cytokinesis. Increases in the cell function are associated with changes in the arrangement of the cytoskeleton of quite a different nature, in particular in the regions of the cytomembrane, the cytocentre, including the Golgi dictyosomes and neighbouring portions of the rough endoplasmic reticulum, at sites of endocytosis and exocytosis and polarization and orientation, and in conjunction with intracytoplasmic translocations after the fusion of macrophages to form multinucleate giant cells. We do not consider the findings described here to be a sort of more or less static compartimentalization phenomenon, but, rather, believe them to bear a causal relationship to the functional dynamism of highly activated and specially differentiated macrophages, epithelioid cell equivalents, epithelioid cells and giant cells. Moreover, they are suggestive of function-dependent, intimate interactions of the individual cytoskeletal components. The experimental, reversible disturbance by the use of colchicine leads in macrophages to a transient loss of structural and functional identity with drastic alterations of microtubules and vimentin filaments.