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T Plesner

Publications and source records attributed to T Plesner.

At least 37 records · Page 2Linked to original sources
PubMed1989

Novel primary thymic defect with T lymphocytes expressing gamma delta T cell receptor.

Flow cytometric analysis of the peripheral blood mononuclear cells in a six year old girl with a primary cellular immune deficiency showed a normal fraction of CD3 positive T cells. Most (70%) of the CD3 positive cells, however, expressed the gamma delta and not the alpha beta T cell receptor. Immunoprecipitation and sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) showed that most of the gamma delta T cell receptors existed as disulphide-linked heterodimers. Proliferative responses to mitogens were severely reduced, but specific antibody responses after vaccination could be detected. A thymic biopsy specimen showed severe abnormalities of both the thymic lymphoid and epithelial component with abortive medullary differentiation and almost an entire lack of Hassall's corpuscles. This patient represents a case of primary immune deficiency syndrome not previously described. Thymic deficiency associated with a high proportion of T cells expressing the gamma delta T cell receptor has been described in nude mice, and it is suggested that the immune deficiency of this patient may represent a human analogue.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

Identification of alpha beta and gamma delta T cell receptor-positive cells.

Two lineages of T lymphocytes bearing the CD3 antigen can be defined on the basis of the nature of the heterodimeric receptor chain (alpha beta or gamma delta T cell receptor (TCR) expressed. Precise identification of alpha beta and gamma delta TCR+ cells is essential when studying the tissue distribution and function of these different T cells. In immunofluorescence studies gamma delta TCR+ cells have been identified as CD3+WT-31- or CD3+CD4-CD8- cells. However, this may not be the optimal procedure because gamma delta TCR+ cells are weakly WT-31+, and some are CD8+. The aim of this study was to evaluate a panel of monoclonal antibodies (MoAb) directed against different chains of the TCR-T3 complex for a more precise identification of alpha beta+ and gamma delta TCR+ cells in flow cytometric studies. We found that the MoAb anti-Ti-gamma A and delta-TCS-1, recognizing the TCR-gamma and the TCR-delta chain respectively, only reacted with a subpopulation of gamma delta TCR+ cells, whereas another TCR-delta chain recognizing MoAb anti-TCR-delta 1 reacted with all gamma delta TCR+ cells. All MoAb reported to belong to the CD3 group reacted with both alpha beta TCR+ and gamma delta TCR+ cells as expected. Our results indicate that all gamma delta TCR+ cells can be identified with the MoAb anti-TCR-delta 1. Because no MoAb recognizing the TCR-alpha or TCR-beta chains at the cell surface of intact cells are yet available, we suggest that alpha beta TCR+ cells could be identified as CD3+ anti-TCR-delta 1-cells.

Antibodies, Monoclonal↗
PubMed1988

Characterization and expression of the human T cell receptor-T3 complex by monoclonal antibody F101.01.

A murine monoclonal antibody (MoAb) F101.01 reacting with the T cell receptor (TCR)-T3 complex is presented. Immunohistological studies showed that F101.01 specifically stains T-zone lymphocytes in lymph nodes, tonsils, and splenic tissue. Two-colour immunofluorescence and flow cytometry demonstrated co-expression of the antigen defined by F101.01 and the pan-T cell antigens defined by CD2, CD3, CD5, and CD7 antibodies. Cells stained with CD4 and CD8 antibodies were both included in the F101.01-positive population, whereas CD16-positive natural killer cells (NK), B cells (CD19 and CD20), and myeloid cells (CD13 and CD33) were excluded. The target antigen of F101.01 co-modulated with the CD3-defined antigen (T3) and the TCR recognized by the MoAb WT-31. CD3 antibody and WT-31 both blocked binding of F101.01. F101.01 precipitated the TCR-T3 complex from lysates of 125I-labelled peripheral blood mononuclear cells (PBMC) and HPB-ALL, when the lysate was prepared with a detergent (digitonin) that conserves the TCR-T3 complex. FACS analysis of T cells from a patient with a T cell immunodeficiency demonstrated that delta-TCS-1-CD3+CD4+ and delta-TCS-1-CD3+CD8+ cells were brightly F101.01+, whereas a large subpopulation of delta-TCS-1+CD3+CD4-CD8- cells were weakly F101.01+. We conclude that F101.01 recognizes a conformational epitope of the TCR-T3 complex and that it reacts with the alpha beta TCR-T3 and the gamma delta TCR-T3 complexes with different intensities.

Antibodies, Monoclonal↗
PubMed1988

The CLL2 study: preliminary results of flow cytometry immunophenotyping in the first 500 patients.

In the period 1984-1987, 500 consecutive, newly diagnosed patients with chronic lymphocytic leukaemia (CLL) have been registered in the still open Danish CLL2-study. As part of patient work-up, the immunological phenotype was established in all patients by immunofluorescence microscopy, and in 458 patients also by flow cytometry, with a panel of polyclonal and monoclonal antibodies. The majority of cases exhibited a CD5-pos, SmIgMD-pos phenotype with faint SmIg-fluorescence, and there is as yet no significant difference in survival between SmIgD-pos and SmIgD-neg cases. Seventy cases were FMC7-pos, a marker associated with a higher B-cell differentiation, and this was significantly correlated with stronger SmIg fluorescence intensity and splenomegaly (Rai stage II). The survival of the FMC7-pos patients was not significantly different from that of the FMC7-neg. Thus, in this preliminary phenotype analysis of the first 500 patients in the CLL2 study, no important prognostic subgroups were detected, although this might be due to the still short observation time (median observation time 532 days).

Denmark↗
PubMed1987

Lack of prognostic significance of T-lymphocyte subset counts in B-cell chronic lymphocytic leukaemia.

In the 50 newly diagnosed, unselected, untreated B-CLL patients, the absolute numbers of blood T cells, T-helper cells, and T-suppressor/cytotoxic cells were by flow cytometric counting of mononuclear cells labelled with the monoclonal antibodies Leu5 (T cells), Leu3a (T-helper cells), and Leu2a (T-suppressor/cytotoxic cells). These estimations and the serum concentrations of IgG, IgA, and IgM were correlated to clinical stage (International Workshop System) and pretreatment observation time. For all patients together, the mean counts of Leu5+, Leu3+, and Leu2+ cells were significantly increased compared with the mean counts in 12 healthy controls (Mann-Whitney). In patients with advanced disease (stage B + C), both T-subset mean cell counts were significantly increased, whereas in patients with early-stage disease (stage A), although some high T-helper cell counts were noted, only the T-suppressor/cytotoxic mean cell count increase reached significance. Thus a trend was observed of a more frequent T-suppressor/cytotoxic cell predominance in early-stage disease, which is the opposite of the findings in most other prognostic studies. However, there was no significant difference in pre-treatment observation time according to T-helper: T-suppressor cell ratio below vs. above 1.0, irrespective of stage, whereas according to clinical stage, the pretreatment observation time in stage A was highly significantly longer than in stage B + C (logrank test). Thus, no independent prognostic significance of T-subset counts was found as judged by pretreatment observation time. No correlation was found between the occurrence of hypogammaglobulinaemia, T-subset ratios or T-subset counts.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1987

Alpha-interferon induces enhanced expression of HLA-ABC antigens and beta-2-microglobulin in vivo and in vitro in various subsets of human lymphoid cells.

The effect of cloned alpha-interferon (alpha-IFN) on the in vitro and in vivo expression of HLA-ABC antigens and beta-2-microglobulin (beta-2-m) on subpopulations of human lymphoid cells was studied by flow cytometry. Mononuclear cells isolated from patients and cell cultures were labelled with saturating amounts of FITC conjugated monoclonal anti-HLA-ABC or anti-beta-2-m. Phycoerythrin conjugated monoclonal antibodies were simultaneously used for the selection of T lymphocytes. T helper lymphocytes, T suppressor lymphocytes, B lymphocytes and monocytes. In vitro, alpha-IFN induced a significant increase of beta-2-m on all subsets investigated. The increase was more pronounced on B lymphocytes (64%) and monocytes (69%) than on T lymphocytes (39%) (P less than 0.01). Also the pretreatment level of beta-2-m was found to be higher on B lymphocytes (0.64 arbitrary units (a.u.)) and monocytes (0.65 a.u.) than on T lymphocytes (0.24 a.u.) (P less than 0.001). In vivo, the expression of both HLA-ABC antigens and beta-2-m was studied in three patients 24 h after administration of 50 x 10(6) units alpha-IFN/m2 i.m. HLA-ABC antigens were significantly (P less than 0.05) increased on all subsets investigated, except for T suppressor lymphocytes. The increase in beta-2-m only reached significance on T lymphocytes. T helper lymphocytes and monocytes (P less than 0.02). At 48 h after administration of alpha-IFN, expression of HLA-ABC antigens and beta-2-m approached pretreatment levels. Enhanced expression of HLA-ABC antigens and beta-2-m could be reinduced by treatment of alpha-IFN on day 7.

B-Lymphocytes↗
PubMed1987

Modification of beta-2-microglobulin in sera from patients with small cell lung cancer: evidence for involvement of a serine protease.

Modification of beta-2-microglobulin has been shown to occur in vitro in serum of patients suffering of small cell lung cancer, where it clearly correlated to the clinical course of disease. The cause of serum beta-2-microglobulin modification occurring in these patients is investigated in the present study. This revealed that modification of beta-2-microglobulin is due to cleavage by a serine protease, which is dependent on divalent cations and has a trypsin-like specificity. The process showed the following characteristics: pH optimum at 8.5, heat inactivation by incubation at 56 degrees C for 20 min and temperature optimum at 20 degrees C.

Carcinoma, Small Cell↗
PubMed1986

Simultaneous presence of translocations t(14;18) and t(2;8) in a case of chronic lymphocytic leukemia.

We report a patient with classical chronic lymphocytic leukemia of IgM kappa phenotype and a stable clinical course, in which repeated chromosome analyses of blood lymphocytes revealed the coexistence of t(14;18), a marker often associated with follicular low grade lymphocytic lymphomas, and t(2;8), a variant of the t(8;14) typically seen in Burkitt's lymphoma. Both these translocations involve immunoglobulin gene regions, the t(2;8) being almost always found in patients with kappa light chain restriction. However, in an EBV-immortalized cell line of this patient, most karyotypes contained t(14;18) alone, without the t(2;8). This suggests that t(14;18) was the primary cytogenetic event, and that t(2;8) evolved subsequently. As a secondary cytogenetic event, the t(2;8) may not share the grave clinical consequences of a primary t(2;8) as seen in Burkitt's lymphoma and related disorders.

Aged↗
PubMed1985

Lymphocyte subsets in patients with compositae oleoresin dermatitis and increased UVA sensitivity during treatment with azathioprine.

Four patients with severe contact dermatitis resulting from compositae oleoresin were found to have increased sensitivity to ultraviolet light. All showed a clear reduction of Leu-3a-positive lymphocytes (T helper/inducer cells) and cells expressing the Ia phenotype in their blood. The numbers of T suppressor/cytotoxic (Leu 2a) lymphocytes, monocytes and B lymphocytes were within the normal range. Treatment with azathioprine (150 mg daily) improved the eczema. The number of Leu-3a-positive lymphocytes normalized during therapy, but the number of Ia-positive cells did not.

Aged↗
PubMed1985

Immunological markers in acute leukaemia.

61 acute leukaemias were classified by both immunological and morphological criteria. In 58 (95%) of the cases correlation was found between the immunological and morphological diagnosis. In 3 (5%) cases, no correlation was found between the immunological subclasses and the FAB-subgroups in ALL. Neither was a correlation found between FAB-subclasses in AML and reaction with myeloid antibodies other than MY-7 which did preferentially react with M4 and M5 leukaemia.

Adult↗
PubMed1985

Sézary syndrome: phenotypic and functional characterization of the neoplastic cells.

Phenotypic properties of the neoplastic cells in skin, blood and lymph node specimens from 5 patients with the Sézary syndrome were examined by immuno-enzymatic and -fluorescence labelling of cells and tissue sections with a monoclonal antibody panel. In 3 cases, the in vitro functional properties of the neoplastic cells (isolated from blood specimens) were also analysed using a reverse plaque-forming cell assay. 3 different immunological categories were identified as follows: T-helper/inducer neoplasms (3 patients); T-suppressor/cytotoxic neoplasms (1 patient); and neoplastic T-cells demonstrating characteristics consistent with a concept of their derivation from inducible suppressor T-cells (1 patient). These data provide conclusive evidence that Sézary syndrome is heterogeneous with respect to the immunological characteristics of the neoplastic cells.

Aged↗
PubMed1985

Expression of an antigen defined by a monoclonal antibody (SA-1) on normal and malignant cells.

A monoclonal antibody (SA-1) has been characterized. The antibody was derived from the fusion of the X-63 myeloma cell-line with splenocytes from a mouse immunized with human acute megakaryoblastic leukaemia cells. The antibody reacted with blast cells from 65% of patients with AML without correlation to morphologic classification. The antibody further reacted with a subset of myeloid cells from normal bone marrow, and with peripheral neutrophil granulocytes. In lymph nodes the antibody showed reactivity with subsets of dendritic reticulum cells. In skin biopsies the antibody reacted with subsets of Langerhans cells, subsets of indeterminate cells and activated T-lymphocytes. The antigen was not expressed on non-activated T-lymphocytes. Neither was it expressed on B-lymphocytes, erythrocytes, platelets nor blast cells from patients with ALL. The antigenic target for the antibody SA-1 was a surface exposed polypeptide (mol. wt. 15 000 D).

Antibodies, Monoclonal↗
PubMed1985

Enhanced expression in vivo of HLA-ABC antigens and beta 2-microglobulin on human lymphoid cells induced by human interferon-alpha in patients with lung cancer. Enhanced expression of class I major histocompatibility antigens prior to treatment.

The effect of cloned human interferon-alpha (IFN-alpha) on the expression of HLA-ABC antigens (HLA-ABC) and beta 2-microglobulin (beta 2m) on human peripheral lymphoid cells in vivo was studied by cytofluorometry using monoclonal antibodies and fluorescein-labelled rabbit anti-mouse immunoglobulin. A significant increase in the mean fluorescence intensity of HLA-ABC (median 59%, P less than 0.001) and beta 2m (median 57%, P less than 0.001) on small lymphoid cells was observed 24 h after initiation of IFN-alpha treatment (50 X 10(6) units IFN-alpha/m2 three times a week). The enhanced expression of these antigens in vivo was found in 11 of 12 examined patients with primary bronchial carcinoma. A concomitant increase in serum beta 2m (median 90%, P less than 0.001) was found in all patients. In contrast the amount of cell-associated HLA-ABC and beta 2m remained unchanged (P greater than 0.1 and P greater than 0.5, respectively) by day-to-day analysis of an untreated healthy control group. An increased expression of both HLA-ABC (mean 55%, P less than 0.0005) and beta 2m (mean 23%, P less than 0.01) was also observed prior to treatment in the lung cancer patients when compared to a group of age matched healthy individuals. Treatment with IFN-alpha caused a significant redistribution of mononuclear cells resulting in both absolute and relative lymphopenia. Pre-treatment lymphocyte counts were 1.09 X 10(9)/1 (range 0.49-1.73), post-treatment counts were 0.55 X 10(9)/1 (range 0.39-1.06).

Adult↗
PubMed1984

Modification of beta 2-microglobulin in serum from patients with small cell carcinoma of the lung--correlation with the clinical course.

A beta 2-microglobulin (beta 2m) 'modifying activity' has been demonstrated by crossed radioimmunoelectrophoresis of serum. The activity could be estimated by planimetry and expressed in arbitrary units (A.U.). Elevated values of beta 2m 'modifying activity' (greater than 0.30 A.U.) has been demonstrated in 49 of 54 patients with small cell lung cancer. The values returned to normal (less than 0.30 A.U.) in eight of the ten patients achieving complete remission (CR) and in three of seven patients achieving partial remission (PR) after chemotherapy. The decrease was more pronounced (median 0.56 versus 0.16, p less than 0.01) in patients achieving CR compared with patients achieving PR. Relapse was accompanied by rising values in 11 of 15 patients monitored during chemotherapy. In nine of these patients abnormally high values of beta 2m 'modifying activity' was demonstrated more than 1 month before clinical or radiological evidence of disease progression. Total serum beta 2m was measured by radioimmunoassay. Elevated values (greater than 200 nmol/l) was found in 14 of 48 patients with small cell lung cancer. No correlation with the clinical course was found in patients monitored during chemotherapy. Estimation of total beta 2m is of no clinical value in small cell lung cancer. Estimation of beta 2m 'modifying activity, provides clinically relevant information, but is too laborious for routine clinical application. The biochemical process underlying this phenomenon should be studied further to allow development of a more simple test.

Adult↗