Immunology and cellular biology of Hodgkin's disease.
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.
Slivnick
D J
DJ
Section of Hematology/Oncology, Loyola University Stritch School of Medicine, Maywood, Illinois.
Nawrocki
J F
JF
Fisher
R I
RI
D000938:Antigen-Presenting Cells / Q000473:pathology; D000943:Antigens, Differentiation / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis; D014408:Biomarkers, Tumor / Q000032:analysis; D002460:Cell Line; D006689:Hodgkin Disease / Q000150:complications / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular; D007153:Immunologic Deficiency Syndromes / Q000209:etiology; D007376:Interleukin-2 / Q000172:deficiency; D008565:Membrane Proteins / Q000032:analysis; D009363:Neoplasm Proteins / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
D000943:Antigens, Differentiation; D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; D007376:Interleukin-2; D008565:Membrane Proteins; D009363:Neoplasm Proteins