Apoptosis versus polemosis. Different mechanisms leading to non-necrotic cell death.
Apoptosis is a physiological auto-suicidal, genetically-induced cell deletion process of senescent effete normal cells. Apoptosis guarantees genetic fidelity, minimizes phenotypic variation and eliminates genotypic alteration. The auto-destruction-induced by a cascade of caspases--results in the breakdown of normal cells and the formation of apoptotic bodies. Those bodies are rapidly phagocytized by macrophages and internalized by cells of the same type. On the other hand, polemosis (from Greek polemos: war) is a more dynamic mechanism of cell destruction between two different cell systems. Polemosis is focal, haphazardly distributed at the time of observation, probably erratic and influenced by the chemotactical attraction of committed lymphocytes by neoplastic cells. Polemosis is implemented by the interaction of the Fas-Fas ligand compulsory cellular system of self-defence. The end result of that struggle is manifested by the destruction of committed lymphocytes and the appearance of polemotic bodies (nuclear fragmentation with or without cytoplasmic remnants). The question arises as to whether polemotic bodies are also engulfed by macrophages, as is the case with apoptotic granules. In this work, the possible association between CD68-positive macrophages and intraepithelial polemotic bodies was investigated in sections from 50 colorectal adenomas. Polemotic bodies were found in groups of dysplastic cells in 84% (n=42) of the 50 adenomas, but none of them showed an accumulation of CD68 macrophages around the polemotic bodies. As polemotic bodies (autologous T-cells DNA) are not engulfed by macrophages it is hypothesized that the DNA of these bodies might be incorporated into the nuclei of dysplastic cells. This would satisfy the avidity of the DNA of rapidly proliferating dysplastic cells, a process that takes place, unremittingly, at any given time.
Rubio
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CA
Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and Hospital, 171 76 Stockholm, Sweden. Carlos.Rubio@onkpat.ki.se
D000236:Adenoma / Q000473:pathology*; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D017209:Apoptosis / Q000502:physiology*; D016923:Cell Death / Q000502:physiology*; D015179:Colorectal Neoplasms / Q000473:pathology*; D006801:Humans; D008264:Macrophages / Q000473:pathology; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; C067980:CD68 antigen, human; D000097382:CD68 Molecule