Implications of persistent T cell abnormalities for the etiology of Hodgkin's disease.
Untreated patients with Hodgkin's disease are known to have significant impairment of cellular immunity. Recent studies have demonstrated that effector T cells from these patients have increased sensitivity to the suppression mediated by two normal immunoregulatory cells, ie, suppressor monocytes and suppressor T cells. Thus, increased sensitivity to suppression may be a common cause of multiple abnormalities of cellular immunity. Patients achieving long-term disease-free survival after chemotherapy have also been studied. Although they are no longer anergic, they have persistent reductions in peripheral blood E rosettes and T cell proliferation. Increased sensitivity to suppressor monocytes and T cells also persists. These abnormalities do not appear to be caused by the treatment since they were not detected in diffuse histiocytic lymphoma patients surviving after similar chemotherapy. Immunologic studies in family members are required to determine whether these abnormalities are a permanent immunologic deficit acquired only with the development of Hodgkin's disease or an inherited characteristic that predisposes a patient to develop Hodgkin's disease.
D003208:Concanavalin A / Q000494:pharmacology; D006689:Hodgkin Disease / Q000276:immunology* / Q000401:mortality; D006801:Humans; D007111:Immunity, Cellular; D008213:Lymphocyte Activation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D008223:Lymphoma / Q000188:drug therapy / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D003208:Concanavalin A