Macrophages are a source of many important mediators of wound repair. It was the purpose of this study to see if light could stimulate the release of these mediators. In this study an established macrophage-like cell line (U-937) was used. The cells were exposed in culture to the following wavelengths of light: 660 nm, 820 nm, 870 nm, and 880 nm. The 820-nm source was coherent and polarised, and the others were non-coherent. Twelve hours after exposure the macrophage supernatant was removed and placed on 3T3 fibroblast cultures. Fibroblast proliferation was assessed over a 5-day period. The results showed that 660-nm, 820-nm, and 870-nm wavelengths encouraged the macrophages to release factors that stimulated fibroblast proliferation above the control levels, whereas the 880-nm wavelength either inhibited the release of these factors or encouraged the release of some inhibitory factors of fibroblast proliferation. These results suggest that light at certain wavelengths may be a useful therapeutic agent by providing a means of either stimulating or inhibiting fibroblast proliferation where necessary. At certain wavelengths coherence is not essential.
Normal human serum contains autoantibodies to a wide range of cellular and serum proteins. IgG autoantibodies to cell membrane proteins spectrin, syndein (Band 2.1), Band 3 degradation products, and the senescent cell antigen are among them. Physiologic autoantibodies to the senescent cell antigen, a approximately 62 000 dalton glycopeptide derived from Band 3, initiate removal of senescent, damaged, and stored cells in vivo. The senescent cell antigen is one of the two Band 3 degradation products (Mr approximately 66 000 and 62 000) observed in freshly prepared ghosts. Since the senescent cell antigen is observed on red cells aged in situ, data suggest that Band 3 undergoes proteolysis in situ. IgG eluted from blood stored for transfusion binds to the senescent cell antigen. The amount of IgG on red cells increases during storage suggesting accumulation of the senescent cell antigen. Autoantibodies to other cell and serum proteins are discussed as possible regulators of homeostasis. The effect of age on physiologic autoantibodies is reviewed.
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