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Hematol Oncol Clin North Am. 1989 Jun;3(2):205-20.

Immunology and cellular biology of Hodgkin's disease.

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Section of Hematology/Oncology, Loyola University Stritch School of Medicine, Maywood, Illinois.


Patients with Hodgkin's disease, either untreated or in remission, exhibit a persistent defect in cellular immunity. This cellular immune defect appears to be the result of increased sensitivity to suppressor monocytes and T-suppressor cells, in addition to abnormal Interleukin-2 production. T-lymphocyte function is abnormal in patients with advanced disease. The precise origin of Reed-Sternberg and Hodgkin's cells is unknown. Reed-Sternberg cells function as antigen-presenting cells and as accessory cells in mitogen-induced T-cell proliferation. They have properties in common with dendritic cells and activated lymphocytes. L428 cells express a transformation-associated phosphorylated transmembrane protein, with properties of a growth factor receptor, that may play a role in tumorigenic transformation.

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