Frederick R. Davey

Hodgkin's disease: intramedullary phagocytosis with pancytopenia.

Excerpt Bone marrow failure as a result of marrow involvement has been considered the major cause of pancytopenia in patients with Hodgkins disease. We describe here the case of a patient with lym...

Non‐Hodgkin's lymphoma limited to the larynx

A case of primary laryngeal non‐Hodgkins lymphoma is detailed, with a review of the reports in the English literature on this rare site of presentation. Symptoms at onset generally include hoarseness, and may be observed up to 60 months prior to diagnosis. Four of the five cases classified by the Rappaport system are of diffuse histology. The histologic distinction of true lymphoma from pseudolymphoma, which may mimic lymphoma both grossly and microscopically, is reviewed. Local radiotherapy is a curative treatment of choice, with 16 of 18 cases disease‐free throughout follow‐up.

Peripheral blood monocytes in the autologous mixed lymphocyte reaction.

Abstract Non-T lymphocytes stimulate T cells in the autologous mixed lymphocyte reaction (AMLR). Peripheral blood monocytes represent approximately 20% of the non-T cell population. Because monocytes have been shown to be necessary for allogeneic mixed lymphocyte reactions (MLR), we evaluated their necessity in the AMLR. Mononuclear cells from residuals of plateletpheresis were obtained from 18 donors. Enriched T cell, B cell, and monocyte populations were obtained by the centrifugation of mononuclear cell suspensions previously mixed with sheep erythrocytes and by the removal of adherent cells following multiple incubations on plastic plates. T cells were used as responding cells in AMLR. The stimulating cells were B cells alone, monocytes alone, and combinations of varying percentages of B cells plus monocytes. The AMLR was measured on several culture days to determine the timeof maximal proliferation. The mean peak proliferative response was found on culture day 10 using 50% B cells and 50% monocytes as the stimulating cell population. No significant difference was seen between the use of mitomycin C-treated and untreated monocytes. AMLR reactivity was compared to HLA-DRW phenotype of the donors. The magnitude of the proliferative responses was widely varied and appeared to fall into four groups. Regardless of the grouping, the presence of up to 50% monocytes was shown to provide maximal proliferation. Cells from various individuals yielded different proliferative rates in AMLR, but repeated AMLR at different times on the same individual gave a similar response.

Depressed stimulation in the MLR by B lymphocytes in chronic lymphocytic leukemia: Failure to demonstrate a suppressor cell

Abstract Unfractionated peripheral blood lymphocytes and B-cell enriched fractions from patients with chronic lymphocytic leukemia (CLL) were compared with similar populations from normal donors for their ability to stimulate allogeneic cells in the mixed lymphocyte reaction (MLR). Both unfractionated lymphocytes and enriched B cells from patients with CLL stimulated allogenetic lymphocytes poorly. This poor stimulation did not appear to be the result of low numbers of peripheral blood monocytes in the CLL lymphocyte populations, nor was it due to a shift in the kinetics of the MLR. To determine if a suppressor cell in patients with CLL was affecting the response of allogeneic cells, T- and B-enriched lymphocyte populations from these patients were added as third-party cells to a normal MLR. In five experiments, no suppression of a normal MLR was observed. In addition, plastic adherent and plastic nonadherent lymphocyte populations from patients with CLL were assayed for their ability to stimulate normal lymphocytes in a MLR and to function as suppressor cells in a normal MLR. Both of these subpopulations failed to function as good stimulating cells and to demonstrate suppressive activity in a MLR. Thus, the poor proliferative response observed in a MLR composed of normal responding lymphocytes and CLL-stimulating lymphocytes is probably due to an intrinsic defect in the CLL B lymphocyte.

Function of lymphocyte subpopulations in chronic lymphocytic leukemia. Activity in the allogeneic and autologous mixed lymphocyte reaction

Lymphocyte subpopulations from patients with chronic lymphocytic leukemia (CLL) and from normal age‐matched controls were evaluated for their ability to participate in allogeneic and autologous mixed lymphocyte reactions (MLR). Unfractionated and T enriched lymphocyte populations from normal age‐matched controls responded well to allogeneic stimulation. T enriched lymphocytes from patients with CLL also responded to allogeneic lymphocytes. B enriched lymphocytes from normal age‐matched individuals produced a stronger stimulus in the allogeneic MLR than did unfractionated mononuclear cell populations. Unfractionated and B enriched lymphocyte subpopulations from patients with CLL were poor stimulators in the allogeneic MLR. In normal age‐matched controls T enriched lymphocyte subpopulations were able to respond to autologous B enriched lymphocytes. Autologous mixed lymphocyte cultures from patients with CLL failed to demonstrate any activity.

Splenic alterations in hairy‐cell leukemia: II. An electron microscopic study

Spleens from nine patients with hairy‐cell leukemia (HCL) were studied for ultrastructural alterations. In all cases, hairy cells with typical ultrastructural characteristics were observed within splenic cords and sinuses. Hairy cells had numerous cytoplasmic processes that interdigitated with cytoplasmic processes of other hairy cells. Hairy cells also adhered to sinus endothelial cells and ring fibers and protruded into spaces between endothelial cells. Some normal sinuses were filled with aggregated hairy cells. Other sinuses appeared dilated. Many sinuses were lined by hairy cells that covered thinned endothelial cells and ring fibers. In these abnormal sinuses, endothelial cells were decreased and many appeared injured. The splenic cords were expanded by an infiltration of hairy cells and by large blood‐filled spaces. These findings suggest that hairy cells adhere to many cell surfaces, produce endothelial cell injury and death, and impede the venous flow of blood in the spleen. All of the factors appear to influence the formation of the abnormal splenic sinuses and the blood‐filled spaces that characterize HCL.

T-lymphocyte function in B-cell chronic lymphocytic leukemia

Abstract Unfractionated and T-enriched lymphocyte populations from patients with chronic lymphocytic leukemia (CLL) were compared to similar lymphocytic populations from normal age-matched controls for their ability to respond to phytohemagglutinin. The T-enriched lymphocyte populations from patients with CLL and from controls were also evaluated for their capacity to respond to allogeneic antigens in mixed lymphocyte cultures and to generate cytotoxic effector cells. Although unfractionated peripheral blood lymphocytes from CLL patients responded poorly to phytohemagglutinin, T-enriched lymphocyte populations responded normally to PHA and to allogeneic antigen. In addition, T-enriched lymphocytes from patients with CLL were able to from cytotoxic effector cells normally. Therefore, T-lymphocyte function in patients with CLL as measured by these three assays is normal.

B Lymphocyte Function in B Cell Chronic Lymphocytic Leukaemia

Summary. B‐enriched lymphocyte populations from patients with chronic lymphocytic leukaemia (CLL) were compared to B‐enriched lymphocyte populations from normal age‐matched controls for their ability to stimulate a proliferative response and to generate cytotoxic cells in allogeneic mixed lymphocyte cultures (MLC). The proliferative responses of MLCs were less than normal when the stimulating cells originated from B cells of patients with CLL. The degree of stimulation provided by the B cells from the patients with CLL inversely correlated with the peripheral white cell count. Lymphocytes from patients providing a poor stimulatory signal in the MLC tended to have less‘Ia‐like’antigen than lymphocytes giving a moderate level of stimulation. B lymphocytes from patients with CLL which stimulated poorly in the MLC also failed to generate specific cytotoxic cells even when provided with a normal proliferative trigger. These data suggest that B lymphocytes from cases of CLL with markedly elevated leucocyte counts may have a diminished concentration of both‘Ia‐like’and serum defined antigens.

The presence of Burkitt‐like cells in non‐Burkitt's neoplasms

In four cases, the morphology of neoplastic cells from the peripheral blood and bone marrow suggested the diagnosis of American Burkitts lymphoma or acute lymphocytic leukemia (French‐American‐British‐Classification; FAB‐L3). Cytochemical and immunologic studies, however, indicated that the neoplastic cells in one case were characteristic of acute lymphocytic leukemia (non‐B, non‐T‐cell type); in another case, metastatic carcinoma; and in two cases acute myelomonocytic leukemia. We conclude that cytochemical and immunologic cell markers are necessary for the diagnosis of American Burkitts lymphoma. In addition, neoplastic cells simulating lymphoblasts of acute lymphocytic leukemia, FABL3 may derive from non‐B lymphocytic lineage. Cancer 50:1770, 1982.

Studies of mixed lymphocyte reactions, surface B cell antigens, and intracytoplasmic immunoglobulins in “null cell” acute lymphocytic leukemia

Lymphoblasts from “null cell” acute lymphocytic leukemia (ALL) were analyzed for the pattern of proliferation displayed in a mixed lymphocyte reaction (MLR), the presence of a B cell surface antigen, and for the presence of intracytoplasmic immunoglobulin (ICIg). “Null cell” ALL was defined by cytologic and cytochemical criteria and by the absence of spontaneous rosette formation and surface membrane immunoglobulin in cell suspensions of the malignant lymphocytes. In eleven of fourteen patients the proliferative characteristics of lymphoblasts in the MLR were similar to those observed with normal B enriched lymphocytes. In eleven cases studied, anti‐B cell serum reacted with a majority of the lymphoblasts. None of the ten cases examined displayed ICIg in the lymphoblasts. We conclude that the “null” lymphoblast from most cases of ALL is a B cell in an early stage of development.