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Biomedical subjects

T Radaszkiewicz

Publications and source records attributed to T Radaszkiewicz.

At least 109 records · Page 6Linked to original sources
PubMed1984

Imbalance of helper and suppressor T lymphocytes in malignant non-Hodgkin lymphomas: an in situ morphometric analysis.

The number and distribution of reactive T cells within 100 malignant B-cell lymphomas were evaluated in situ by immunomorphometry using stereological methods. Findings were related to histological and clinical parameters. A mean of 2 X 10(4) reactive T cells/microliter tumour tissue was found. This corresponds to 40% of the T-cell content of normal lymphatic tissues. The distribution of reactive T cells within the tumours was diffuse except for centroblastic/centrocytic lymphomas. When evaluating the different histological entities a correlation between number of helper T cells, T helper:T suppressor (TH:TS) ratio and histological subgroups emerged, particularly in non-Hodgkin lymphomas of low-grade malignancy. The highest ratio was found in prognostically favourable subgroups, CLL (2.7 +/- 0.3) and tumour areas of centroblastic/centrocytic lymphomas (2.9 +/- 0.4). In contrast, a significantly lower ratio was found in centrocytic lymphomas (1.4 +/- 0.3) corresponding well to the worst prognosis of this subgroup. The relationship between the number of helper T cells in tumour tissues, TH:TS ratio and prognosis was confirmed and extended by the evaluation of clinical data. It could be shown that, independently of histological criteria, a close correlation exists between the number of T cells, particularly T helper cells within the tumour, TH:TS ratio and clinical course. Patients with a favourable course had 1.4 X 10(4) T helper cells/microliter tumour tissue compared to only 0.8 X 10(4) for patients with an unfavourable clinical course (p less than 0.01); the TH:TS ratio was 2.8 for the favourable and 1.8 for the unfavourable group, respectively (p less than 0.04). In contrast, neither treatment nor tumour stage had a clear-cut influence on the extent of T-cell infiltration.

B-Lymphocytes↗
PubMed1984

[A 60-year-old patient with sialadenitis, pulmonary round foci and vulvar ulcer].

The unusual case of a 60 year-old woman is discussed. She presented with sialadenitis, paresis of the facial nerve, keratoconjunctivitis and ulcus vulvae. Basic anamnestic information revealed primary enlargement of the submandibular gland, fever, otitis, sinusitis and a pulmonary tumour. The serum immunoglobulin E level was raised. In addition to the necrotic granulomas in the lungs, spleen and kidney, characteristic changes were found in the lymph nodes, liver, pancreas and colon.

Cyclophosphamide↗
PubMed1984

Malignant histiocytosis with unusual features. Disseminated intravascular coagulation with severe hyperfibrinolysis, acute polyneuroradiculitis Guillain-Barré, and a unique chromosome abnormality.

The case of a 25-year-old man with the characteristic features of malignant histiocytosis (proliferation of abnormal histiocytic cells with erythrophagocytosis, hepatosplenomegaly, increased serum acid phosphatase, hypercalcemia, and bone pain) is reported. Chromosome studies revealed a near tetraploid karyotype with a pair of marker chromosomes. A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis. Cerebrospinal fluid (CSF) findings were consistent with a diagnosis of Guillain-Barré Syndrome. On the next day, disseminated intravascular coagulation (DIC) with severe hyperfibrinolysis occurred. After intensive chemotherapy, complete remission could be achieved.

Adult↗
PubMed1984

Diagnostic specificity of the monoclonal anti-CALLA antibody VIL-A1 in leukemia and malignant lymphoma.

VIL-A1 is an anti-CALLA antibody which binds efficiently and exclusively to CALLA positive cells. When the cell type specificity of VIL-A1 is studied in acute leukemias and lymphomas, results show that in those leukemias which could be characterized by cytochemical and morphological methods, VIL-A1 reactivity was specific for cells of lymphoid origin. It can therefore be assumed that VIL-A1 positive AUL cells (in this case 4 out of 9 patients) are also lymphoid in origin. In no case were AML blasts found to be positive with this antibody. Seventy-four per cent of the 88 ALL patients were positive (L1 + L2) whereas none in the L3 subgroup were positive, and 48% of CML patients in blastic crisis were positive. Of the low grade non-Hodgkin malignancies, only CB/CC was positive, distinguishing it from the CC type which was negative. Of the high grade lymphomas IB was found to be negative, while the others showed a heterogeneous picture which was not related to other immunological parameters.

Acute Disease↗
PubMed1984

Allosuppressor- and allohelper-T cells in acute and chronic graft-vs-host disease. IV. Activation of donor allosuppressor cells is confined to acute GVHD.

Groups of nonirradiated BDF1 mice were injected with unseparated spleen cells from B10, B10.D2, or DBA/2 donors. The diverse clinical and pathologic symptoms that developed during the course of the ensuing graft-vs-host reaction (GVHR) were related to the functional subsets of donor-T cells activated in the host. The activation of F1-specific donor T suppressor (TS) cells was confined to those GVH F1 mice that developed acute GVH disease (GVHD) (donor B10 or B10.D2). Moreover, activation in these GVH F1 mice of the Lyt-1-2+ donor TS cells sharply preceded the onset of and coincided with (week 2 to 6) the suppressive pathologic symptoms characteristic of acute GVHD, such as pancytopenia and suppression of splenic IgG production. The activation of these alloreactive TS effector cells was briefly preceded by the activation of F1-specific Lyt-1+-2- donor T helper (TH) cells and stimulation of the host's lymphoid tissue. Thus, in acute GVHD, a sequential alloactivation first of donor TH and then of TS cells was found. Those F1 mice that recovered from acute GVHD and developed stimulatory pathologic symptoms showed a concomitant loss of donor TS cell activity. An initial activation of F1-specific Lyt-1 +2- donor TH cells was also found in that parent----F1 combination (donor DBA/2), which failed to develop acute GVHD. Significantly in that combination, the alloactivation of donor TH cells was not followed by activation of significant numbers of donor TS cells. Instead, the DBA/2-injected BDF1 mice directly developed a persistent increase in splenic Ig formation and lupus-like GVHD.

Acute Disease↗
PubMed1983

Phenotypes of human large granular lymphocytes as defined by monoclonal antibodies.

Four monoclonal antibodies VEP8, VEP9, VIM-D5, VIB-C5 against antigens expressed on human mature myeloid cells (polymorphonuclear leukocytes [PMNL] and/or monocytes) as well as on immature cells in the bone marrow were tested for reactivity with cell preparations highly enriched for large granular lymphocytes (LGL). These cells are known to be the main effector cells responsible for natural killer (NK) cell activity in human peripheral blood. Using indirect membrane immunofluorescence (IMF), none of these antibodies showed any reactivity at all. In addition, LGL-enriched cell preparations were tested with the anti-lymphocyte monoclonal antibodies OKT6, anti-Leu1, anti-Leu2a, anti-Leu3a, and anti-human Lyt3, and also with OKM1 antibody. Significant reactivity was found with anti-Leu2a (59 +/- 8%), anti-Lyt3 (55 +/- 4%) and OKM1 (81 +/- 11%) antibodies, whereas T6, Leu1, and Leu3a antigens were less pronounced or missing on LGL. As a further approach, another monoclonal antibody, VEP13, which reacts with LGL, granulocytes but not monocytes and is therefore different in its specificity from OKM1 and OKT10, was used for identification of LGL. The coexpression of antigens as defined by the above-mentioned antibodies and OKT10 on VEP13+ cells was studied. Again, phenotypes similar to those observed on LGL enriched by Percoll gradient centrifugation were found: of VEP13+ cells 84 +/- 6% reacted with OKM1, 82 +/- 5% with OKT10, 52 +/- 17% with anti-human Lyt3, and 48 +/- 14% with anti-Leu2a, whereas VEP8, VEP9, VIM-D5, VIB-C5, T6, Leu1, Leu3a antigens were not expressed on VEP13+ cells. Taken together as an overall evaluation of phenotypic characteristics, our data indicate that LGL cannot be integrated into one of the known lymphocytic or myelomonocytic lineages. LGL show an intermediate phenotype depending possibly on varying differentiation or activation stages of haemopoietic cells. However, the possibility also exists that LGL belong to a separate, yet undefined cell lineage.

Antibodies, Monoclonal↗
PubMed1983

Attempts at standardization of lupus-like graft-vs-host disease: inadvertent repopulation by DBA/2 spleen cells of H-2-different nonirradiated F1 mice.

By induction of a suitable graft-vs-host reaction (GVHR) in nonirradiated, H-2-incompatible F1 mice, one can induce a syndrome strongly resembling systemic lupus erythematosus (SLE). The aim of the present study was to standardize the kind and number of DBA/2 donor cells required for optimal induction of this SLE-like GVH disease (GVHD). Groups of adult (C57BL/10 x DBA/2)F1 (BDF1) mice were injected i.v. with increasing numbers of DBA/2 spleen and lymph-node cells. We found that doses of 100 x 10(6) to 180 x 10(6) spleen and lymph-node cells provided a suitable donor-cell inoculum, whereas doses of donor cells below 100 x 10(6) were suboptimal and doses higher than 180 x 10(6) cells were supraoptimal for the induction of SLE-like GVHD. In a number of those F1 recipients that had received the donor-cell inocula composed of spleen cells, the duration of autoantibody formation was surprisingly brief. This appeared to be due to the fact that these GVH F1 mice were rapidly repopulated by lympho-hemopoietic donor cells. Even after the highest doses of DBA/2 spleen and lymph-node cells administered, this repopulation was not preceded by symptoms of acute GVH disease. Repopulation was avoided and a severe SLE-like disease induced when a mixture deficient in hemopoietic cells, i.e., 280 x 10(6) DBA/2 lymph-node and thymus cells, was used as donor-cell inoculum. Taken together, we reached three conclusions. First, the induction of full-blown SLE-like GVHD depends not only on the injection of a sufficient number of donor T cells but also on the continuous presence of F1 lymphoid cells, which seem to serve as stimulator cells. Second, in addition to the lymphoid hyperplasia and immune-complex glomerulonephritis (ICGN) described previously, the GVHR-induced lesions presenting themselves in the context of SLE-like autoimmunity include a Sjögren-like lymphoid infiltration of the salivary gland, a ubiquitous periarteritis, and a lymphoid infiltration of the bile ducts that is reminiscent of primary biliary cirrhosis. Third, the repopulation by donor cells of nonirradiated, H-2-incompatible hosts need not be accompanied by GVH mortality or symptoms of acute GVHD.

Animals↗
PubMed1982

Results of LSA2-L2 therapy in 26 children with non-Hodgkin's lymphoma.

Twenty-six children with non-Hodgkin's lymphoma (NHL), 17 boys and nine girls, were treated with the LSA2-L2 protocol. Seven children had stage I or II, 16 Stage III and three Stage IV according to Murphy's staging system. Eight children had their primaries in peripheral lymph nodes, eight in the abdomen, six in the mediastinum and four in other sites. All tumors were classified histologically according to four different classifications. Overall disease-free actuarial survival is 53.6%. Complete responders show a disease-free survival of 77.8%. Fourteen children survived for 9-56 months. Included are all seven children with Stage I or II who survive irrespective of histologic type of the tumor. Of the remaining 12 children in Stage III or IV three children died in remission and nine of progressive disease. Eight of these nine patients did not attain complete remission. Whereas four of five children with the convoluted type of NHL survive, four of five patients with the Burkitt's type (small noncleaved follicle center cell lymphomas) died of progressive disease. According to Rappaport's classification, four of six children with diffuse undifferentiated lymphoma (DUL) are dead due to tumour progression. Considering the classification of lymphoblastic lymphomas introduced by Nathwani et al., 23 five of seven children suffering from lymphoblastic lymphomas but only two of eight children with nonlymphoblastic lymphomas belong to the survivors. Therefore histologic findings do hold prognostic significance in our series of children with NHL.

Adolescent↗
PubMed1982

Allosuppressor and allohelper T cells in acute and chronic graft-vs-host disease. I. Alloreactive suppressor cells rather than killer T cells appear to be the decisive effector cells in lethal graft-vs.-host disease.

Splenic T cells from B10 donors were injected into irradiated (B10 x DBA/2)F1 mice. Either 5 or 6 d later, activated donor T cells were recovered from the spleens of these primary F1 (1 degree F1) recipients and transferred to groups of nonirradiated syngeneic F1 (2 degrees F1) recipients. Whereas day-5-activated parental T cells induced the characteristic symptoms of acute graft-vs.-host disease (GVHD) and eventually lethal GVHD, day-6-activated B10 T cells failed to induce acute GVHD but induced symptoms of chronic GVHD. Interestingly, the inability of day-6-activated T cells to induce lethal GVHD could not be ascribed to a lack in anti-F1 T killer cells. The combined results of functional studies indicated that day-6 cells were enriched for alloreactive helper T cells, whereas day-5 cells were enriched for alloreactive suppressor cells. Hence, our findings indicate that acute GVHD and lethal GVHD are caused by alloreactive donor T suppressor but not T killer cells, and that symptoms of chronic GVHD are caused by alloreactive donor T helper cells.

Acute Disease↗
PubMed1981

[Chronic lymphatic leukemia of B-cell type: clinical and morphological investigations for diagnostic differentiation (author's transl)].

Chronic lymphatic leukemia (CLL was diagnosed in 71 patients based on clinical data. Most of the patients were in the stages 0, I and II, only 18% were in the stages III and IV according to Rai. In all cases, the disease was characterized by an increased number of B lymphocytes (B-CLL). The B cells mostly expressed a weak fluorescence intensity when tested for membrane bound immunoglobulins (Ig). In accordance to that, the quantitative measurement of Ig in the serum revealed a decrease of one or more Ig classes in 72% of the patients. No correlation existed between the number of b lymphocytes (and T lymphocytes) or the Ig concentration in the serum and the stage of the disease. To distinguish the CLL from related lymphoproliferative disorders, especially the immunocytic lymphoma, lymph node biopsies were examined histologically and immunomorphologically for intracytoplasmic Ig. This examination confirmed the diagnosis of CLL in 33 out of 40 cases. Six lymph nodes were classified as immunocytic lymphoma of the lymphoplasmacytoid type. In three of the latter, the immunocytic lymphoma was clinically associated with decreased Ig concentrations in the serum. These findings emphasize that the clinically established diagnosis of CLL should be corroborated by immunomorphology.

Adult↗
PubMed1981

Spontaneous rosette formation of pig and guinea pig thymocytes and peripheral blood lymphocytes: influence of proteases, oxidising and reducing agents, cytochalasin B and carbohydrates.

Spontaneous rosette formation (SRF) of pig and guinea pig thymocytes (Th) and thymus derived peripheral blood lymphocytes (PTL) was tested under different experimental conditions. Treatment with different proteases (trypsin, chymotrypsin, protease type VII) showed that SRF of pig Th and PTL is inhibited to a much higher extent than that of guinea pig Th and PTL. Cytochalasin B (CB) inhibited SRF of PTL of both species to a higher degree as compared to Th. Different carbohydrates neither influenced SRF of Th nor of PTL in both species indicating that simple carbohydrates are not the recognized component of SRF receptors. Treatment with oxidising and reducing agents did not influence SRF.

Animals↗
PubMed1981

Proliferation kinetics of Sézary cells.

The proliferation kinetics of neoplastic T cells arising in Sézary syndrome (Sézary cells) are still poorly understood. Kinetic studies with 3H-thymidine as a DNA precursor revealed a low incorporation rate of the nucleotide into Sézary cells obtained from the peripheral blood versus Sézary cells from the skin. Using the double-label autoradiography we determined the duration of single cell cycle phases of blood and cutaneous Sézary cells. The results indicate the almost complete lack of proliferative activity in the blood but a considerable portion of proliferatively active Sézary cells in skin infiltrates. The removal of a large mass of quiescent blood cells by leukapheresis did not affect the proliferative state of the residual peripheral cell population implying that the procedure did not induce the migration of proliferating skin cells towards the blood. Terminally, the disease underwent transition into immunoblastic lymphoma. At this time, the kinetic behavior of the peripheral immunoblasts showed great similarity to that of cutaneous Sézary cells. The findings point towards a common extravascular production site of Sézary cells and immunoblasts probably located in the lymphatic tissue.

Aged↗
PubMed1980

[Malignant and benign lymphomas: histologic classification and immunomorphologic studies. Results of 838 cases].

800 malignant (22.9% Hodgkin's, 77.1% non-Hodgkin's) lymphomas, 22 cases of lymphogranulomatosis X and 16 pseudolymphomas were investigated by histology and immunomorphology. Age- and sex-distribution, localization as well as intracytoplasmic immunoglobulins (Ig) in tumour cells were evaluated. Hodgkin's lymphomas were classified according to Lukes (1971), the non-Hodgkin's lymphomas (NHL) according to the Kiel-classification. Among NHL of low grade malignancy the most common type was chronic lymphocytic leukaemia (CLL) (18%), among the NHL of high grade malignancy the immunoblastic lymphomas (IB) (13%). In IB 5 cases of T-cell type of IB were be identified. 8 cases were classified as "histiocytic" reticulosarcomas. Immunomorphology performed on routinely formalin-fixed, paraffin-embedded tissue sections showed a clear-cut difference between CLL and immunocytic lymphomas (IC): In all IC "monoclonal" Ig could be detected in lymphoplasmacytoid and plasma cells. The most common Ig was of the IgM/K type. 4 IC were turned out as "biclonal" ML detected by the double immunofluorescence. In IB lymphomas less than 50% contained intracytoplasmic Ig mainly of the IgM/K type. In Hodgkin's- and Sternberg cells sometimes IgG, K, lambda and also lysozyme was observed intracytoplasmically. This finding supports the hypothesis of the macrophage origin of these cells. In lymphogranulomatosis X and in lymphoepithelioid cell lymphoma (Lennert's lymphoma) as well as in pseudolymphomas "polyclonal" Ig containing "reactive" plasma cells was demonstrable. Immunomorphology on routine pathological material is able to facilitate differential diagnosis of ML and to elucidate to some extent derivation of ML.

Biomarkers, Tumor↗
PubMed1980

[Histomorphologic examinations of bone marrow of patients with gynecologic malignoma before, during, and after radiotherapy (author's transl)].

The histomorphological changes in the bone marrow were investigated in 9 patients treated by primary irradiation for cervical cancer. Bone marrow specimens were obtained by the Yamshidi puncture technique from the spina iliaca posterior superior after radiotherapy with different radiation dosages, as well as four months after termination of radiotherapy. All patients showed disappearance of almost all the haematopoietic cells in the irradiated area and, with the exception of one patient, no repopularization of the bone marrow or fibrosis. The possible mechanisms leading to these results are discussed and comparisons with the international literature are drawn.

Aged↗