Hodgkin's disease: a war between T-lymphocytes and transformed macrophages?
The interaction between Reed-Sternberg (RS) cells and autogeneic T T cells was investigated. It was found that T cells cytolyse RS cells in the following sequential manner: Stage 1, T cells affix the tips of their microvilli onto target cells, Stage 2, T cells subject cell membranes to tearing, and shearing forces which produce gaps and holes; Stage 3, target cells lyse and T cells "crawl" away. The relationship between the events occurring at the cellular level and those observed clinically are discussed. Hodgkin's disease holds a fascination for clinicians and "bench" scientists alike, perhaps because of the enigma and challenge it represents. It is not surprising, therefore, that many questions go unanswered. For example, we are still addressing ourselves to the following questions: What is the origin of the Reed-Sternberg (RS) cell? If a macrophage, then why do T cells attach to it and what is the nature of the T cell-RS interaction? Why is cellular immunity so often impaired even in patients in the early stages of the disease? Why do patients with Hodgkin's disease sometimes develop autoimmune hemolytic anemia when they are, in fact, immunologically hyporesponsive? In this paper, I shall present evidence which answers a few of these questions and provides hypothetical answers to the others.
D006689:Hodgkin Disease / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007111:Immunity, Cellular; D008264:Macrophages / Q000502:physiology*; D008855:Microscopy, Electron, Scanning; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000502:physiology*