Spectrum of immunodeficiencies with Hodgkin's disease.

Abnormalities of in vitro immunoglobulin synthesis by peripheral blood lymphocytes from untreated patients with Hodgkin's disease.

“…Since Ig synthesis induced by PWM is subject to the regulatory activity of monocytes (21,22), the abnormality could be associated with an increase in the number of these cells relative to lymphocytes in MNC suspensions (23). Indeed, using monoclonal antibodies reactive with monocytic cells we could confirm a recent report showing higher concentrations of monocytes in Ficoll-Hypaque MNC suspensions from patients with HD than in controls (20 (27)(28)(29), and antibodies against Epstein-Barr and other viral antigens (30,31) in patients with HD. Depressed Ig synthesis after stimulation with PWM, associated with enhanced spontaneous IgG synthesis, has also been reported in patients with systemic lupus erythematosus (32,33) and Henoch-Sch6nlein purpura (34) and attributed to an excessive B cell stimulation in vivo (35)(36)(37)(38).…”

“…Furthermore, parallel cultures were established with irradiated (2,000 rad) T cells, because this treatment has been shown to remove the majority of suppressor T lymphocyte activity (19). As shown in Table III (20).…”

Immunopathology of Hodgkin’s Disease

“…Another hypothesis is that the inflammatory cell population is recruited into the tumor by production of as yet unidentified lymphokine-like substances [20], A similar phenom enon is observable in a thymoma, a neo plasm of thymic epithelium which 'recruits' nonneoplastic lymphocytes of normal thymic phenotype [53], The interaction be tween Rccd-Stcrnbcrg cells and normal lym phocytes in some way results in the charac teristic clinicopathologic features of Hodg kin's disease. One striking feature of Hodg kin's disease is the defect in cellular immu nity associated with increased suppressor cell activity and progressive lymphocytope nia [54,55], The increase in suppressor cell acivity would appear paradoxical, since the Hodgkin's disease infiltrates are associated with a predominance of helper T cells [46][47][48][49][50]. The helper-to-suppressor cell ratio may be subtly decreased as compared to benign reactive lymphoid hyperplasias, however [47], The presence of defects in cellular im munity even in localized Hodgkin's disease suggests a systemic (?humoral) effect.…”

Defective Lectin-Induced p55kDa-IL2R Expression on Peripheral T Cells in Non-Hodgkin’s Lymphoma Patients

“…However, evidence has mounted that the defective immune status is also found in untreated patients [1-12, 15. 16], Most of these studies have found that the T cell is the apparent site of this defect, which is manifested as an impaired delayed hypersensitivity, a reduced mitogen-induced T cell proliferation and a reduced mixed lymphocyte culture response [1][2][3][4][5][6][7][8][9][10][11][12], Activation by specific antigen or mitogen induces resting T cells to produce IL2 and to express highand low-affinity receptors for this lymphokine [13,14], The interaction of IL2 with high-affinity receptors causes activated T cells to proliferate [13. 14], 1L2 also plays an important role in the growth and differentia tion of B cells in vitro [23,241.…”

“…Peripheral blood T cells obtained from non-Hodgkin's lymphoma patients show no pathological abnormalities on microscopic examination, whereas functional disabil ity of these cells, including reduction in lectin-induced proliferative response, has consistently been reported [1][2][3][4][5][6][7][8][9][10][11][12]. Opportunistic infections are often found in patients with non-Hodgkin's lymphoma, implying that their immune status is profoundly suppressed.…”