Impaired Lymphocyte Transformation in Hodgkin's Disease. EVIDENCE FOR DEPLETION OF CIRCULATING T-LYMPHOCYTES

Autologous Mixed Lymphocyte Reaction in Patients with Hodgkin's Disease

“…Although antibody responses appear to be unimpaired (1,2), patients frequently exhibit defects of T cell-mediated immune functions manifested by diminished delayed hypersensitivity responses (3)(4)(5)(6)(7), impaired ability to reject skin allografts (8)(9)(10), and decreased resistance to certain types of infection (11)(12). Several in vitro functions of peripheral blood T cells have been shown to be impaired, including the blastogenic response to soluble antigens (13)(14)(15), alloantigens (16,17), and plant lectins (2,(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28). Some ofthese defects may be explained by the presence of suppressor monocytes (17,(28)(29)(30) and suppressor T cells (29,31).…”

Quantitation of immunocompetence in Hodgkin's disease.

“…and degree of nonlymphoid cell contamination of the final lymphocyte suspensions obtained from both patients and controls. Moreover, highly pure lymphocyte suspensions have elicited similar results (20). (d) An intrinsic functional abnormality of all PHA-responsive lymphocytes or depletion of these cells (11,20).…”

“…However, quantitation of the defect was not attempted and no correlation was found with svmptomatologv, skin reactivity and absolute lvmnphocvte count. Another sensitive approach is the study of the entire time-course of the PHA response (20) that disclosed abnormal Hodgkin's lymphocyte responses in all patients studied. However, the in vitro abnormality observed over an 8-day incubation period may reflect magnified in vitro cell death as much as refractoriness to mitogenic stimulation.…”

“…(d) An intrinsic functional abnormality of all PHA-responsive lymphocytes or depletion of these cells (11,20). Dilution of T-lymphocytes by chronic lymphatic leukemia cells seems to account for the abnormal PHA transformation seen in this disease (30 (5,6,8) or it may relate to in vivo stimulation leading to PHA refractory T-lymphocytes (11,20), loss of these cells recirculating capacity (33), or their depletion from peripheral blood (11,20,31).…”

“…With disease progression, this initially subtle (and therefore elusive) impairment becomes more pronounced leading to progressive immunoincompetence with loss of immunologic memory (16,21), shortened cell survival reflected by in vitro cell death (5,6,8), and in vivo cell depletion (11,20,31), with ensuing lymphopenia found mostly in far advanced disease (36).…”