Diminished autologous mixed lymphocyte reaction in patients with hodgkin disease: Evidence for non‐t cell dysfunction

Abstract

In the autologous mixed lymphocyte reaction (AMLR), T lymphocytes are stimulated to proliferate by autologous non-T mononuclear cells. In five untreated patients with Hodgkin disease, the AMLR was diminished. In addition, in the same five patients, T cell response PHA was inhibited by a cell in the non-T cell fraction, the response of non-T cells to PWM was diminished, and there was a diminished ability of the non-T cell population to stimulate in allogeneic MLR. However, the response of T cells from patients with Hodgkin disease to allogeneic antigen was normal. The AMLR and allogeneic MLR were then studied in an additional five untreated patients before and after monocyte depletion of the stimulating non-T mononuclear cell population. In this second group of Hodgkin disease patients, the AMLR was again diminished when T cells were incubated either with non-T cells or non-T cells depleted of monocytes. In the Hodgkin patients, monocyte depletion did not alter the T cell response in the AMLR. In the controls, monocyte depletion greatly diminished the proliferative response. The diminished AMLR in untreated Hodgkin disease patients may be the result of a failure of adequate monocyte stimulation of autologous T cells.

Bone marrow and peripheral blood natural killer cell activity in lymphomas. Its response to IL-2

“…In patients with lymphoid malignancies, cell-mediated immunity, partieularly related to T cells [25][26][27], and to macrophagemediated functions [28] commonly exhibits significant alterations. However, very few studies are available dealing with the peripheral blood NK activity in HD and NHL patients.…”

Association of HLA‐DR antigens with the autologous mixed lymphocyte reaction

“…The AMLR has been found to be depressed in a variety of immunodeficiency states, autoimmune diseases and lymphoproliferative disorders (Engleman et al 1980, Wolos & Davey 1980, Zamkoff et al 1982, James et al 1980, Miyasaka et al 1980, Sakane et al 1978. In some disease states, the depressed AMLR is due to an abnormality in T cells, in others a defect in B cells and still others a deficient function of macrophages .…”