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Biomedical subjects

F Herrmann

Publications and source records attributed to F Herrmann.

At least 253 records · Page 14Linked to original sources
PubMed1985

Expression of interleukin 2 receptors and binding of interleukin 2 by gamma interferon-induced human leukemic and normal monocytic cells.

Gamma interferon induced surface expression of interleukin 2 (IL-2) receptors on normal human monocytes and the monocytoid cell lines U937 and HL60. These receptors were detected by anti-IL-2 receptor monoclonal antibodies, and U937 IL-2 receptors were indistinguishable from T lymphocyte IL-2 receptors by immunoprecipitation. Also, U937 IL-2 receptors bound biologically active IL-2. These results suggest a role for monocyte IL-2 receptors in T cell/monocyte interaction during an immune response.

Antibodies, Monoclonal↗
PubMed1985

Human X chromosome markers and Duchenne muscular dystrophy.

Two DNA markers, a random DNA fragment 754 and the cDNA sequence encoding the gene for ornithine transcarbamylase (OTC) have been studied in kindreds segregating for Duchenne muscular dystrophy. 754 and OTC are located close physically to the mutation in the region Xp21 below the breakpoints in two Duchenne females. The genetic distance was found to be approximately 10cM between 754 and DMD (two crossovers in 26 meioses) and to be approximately 10cM between OTC and DMD (two crossovers in 26 meioses). Physical data suggest the order DMD-754-OTC. The frequency of recombination compared to physical distance between these markers and DMD suggests that there may be a hot spot of recombination. The relevance of these observations for the isolation of the DMD mutation and clinical use of these probes is discussed.

Chromosome Mapping↗
PubMed1985

A comparison of membrane marker phenotypes in hairy-cell leukemia and phorbol-ester induced B-cll cells using monoclonal antibodies.

The neoplastic cells from 14 cases of hairy-cell leukemia were investigated in order to determine their membrane phenotype on the basis of their reactivity with a large panel of B-, T-, myeloid/monocytic- and non-lineage restricted monoclonal antibodies. The data were compared to those from monoclonal antibody studies on phorbol-ester (TPA) induced cells from 10 patients with B-type chronic lymphocytic leukemia. The study has so far revealed further evidence for the B-cell nature of hairy-cells leukemia and demonstrates a developmental link between the two cell types, suggesting that hairy-cells represent a more advanced differentiation stage along the B-cell lineage.

Antibodies, Monoclonal↗
PubMed1985

Impaired B lymphocyte reactivity in patients after radiotherapy.

The effect of therapeutic irradiation upon B lymphocyte function was investigated in patients with various malignancies. The test system used was a reverse hemolytic plaque assay, which made it possible to study the activation and differentiation of B lymphocytes into immunoglobulin-secreting cells (ISC). Peripheral blood lymphocytes from normal individuals and patients before and after radiotherapy were stimulated in vitro with the polyclonal B cell activator pokeweed mitogen, and the number of ISC was estimated. B cell reactivity was markedly reduced in those patients who had received irradiation within the last six months. In patients in whom radiotherapy had been terminated more than 12 months before the lymphocytes were tested, B cell reactivity was comparable to that of patients prior to radiotherapy. By means of marker analyses, there was a reduction of B lymphocytes and T lymphocytes in the peripheral blood with a preponderance of T helper cells. Several mechanisms--e.g., reduced or defective B cell differentiation, altered regulatory T-helper or suppressor cell function or activation of suppressive monocytes--could be responsible for impaired B cell reactivity after radiotherapy.

Adult↗
PubMed1985

Abnormalities of B-cell activation and immunoregulation in splenectomized patients.

Using a reverse hemolytic plaque assay as the effector system, we studied B-lymphocyte function in 12 patients after posttraumatic splenectomy, as well as in 25 normal individuals. The time interval between the splenectomy and the immunological studies varied between 2 days and 7 years. Compared to normal individuals, the splenectomized patients had markedly elevated numbers of spontaneous immunoglobulin-secreting cells (ISC) and severely decreased responses to the polyclonal activator pokeweed mitogen. A tendency towards normalization of these abnormalities, especially the high spontaneous ISC levels, could be observed during the time interval extending up to 7 years after splenectomy. In order to characterize the mechanism responsible for the altered immune response in splenectomized patients, co-culture experiments with unseparated and separated lymphocytes were performed. These revealed an impaired T-helper cell capacity as well as an intrinsic B-cell defect. Marker analyses with monoclonal antibodies revealed normal proportions with the exception of OKT 4 positive and B 1 positive cells that identify T-helper/inducer and peripheral B-cells respectively. We conclude that immune dysfunction in peripheral blood lymphocytes of splenectomized patients involves mainly the B-cell as well as the T-helper/inducer-cell population.

Adult↗
PubMed1985

Chronic lymphocytic leukemia B-lymphocytes forming SRBC-rosettes not due to an anti-SRBC activity of monoclonal surface immunoglobulin.

A case of chronic lymphocytic leukemia is described in which large numbers of peripheral blood lymphocytes expressed immunoglobulin on their membrane and rosetted spontaneously with sheep red blood cells (SRBC) at 4 degrees C. They also showed weak staining with a heterologous antiserum against T-cells as well as with a monoclonal antibody (OKT11) with specificity for an epitope associated with the SRBC-receptor, but failed to react with other T-lineage-restricted monoclonal antibodies. The B-cell origin of the leukemic cells was documented by the presence of light-chain-restricted monoclonal surface immunoglobulin, reactivity with various monoclonal anti-B-cell reagents, presence of Ia-like antigens, their capability to synthesize intracytoplasmic immunoglobulin on exposure to phorbol ester TPA, their lack of response to T-cell mitogen PHA, and their inability to help or suppress the allogeneic B-cell response upon PWM stimulation. Extensive blocking studies with both specific antisera and Forsmann antigen-rich guinea pig kidney extracts, which did not prevent SRBC-rosetting, lend support to the hypothesis that SRBC-rosette formation in this case was not attributable to an anti-SRBC affinity of the surface immunoglobulin on the cells. This case will be discussed in relation to the recent finding of SRBC-rosette expression on some cultured chronic lymphocytic leukemia B-lymphocytes.

Aged↗
PubMed1985

Coincident change of cellular function and phenotype in the course of a suppressor T cell acute lymphocytic leukaemia.

The phenotypic and functional characteristics of the leukaemic cells from one patient with T suppressor ALL were studied at the time of diagnosis and in relapse. At the time of diagnosis, the phenotype corresponded to the intermediate stage between the cortical and medullary phases of normal thymocyte differentiation with a high proportion of T8+ cells (E-R+, TdT+, C3bR-, T3-, T4-, T6+, T8++, T10+). Functionally, the cells did not respond to mitogens but mediated strong suppressor activity to allogeneic B-cells, as measured in a reversely haemolytic plaque test. Clinically, the patient exhibited the uncommon feature of hypogammaglobulinaemia. Induction therapy led to complete remission, which continued for 12 months. In the relapse, the phenotype remained essentially stable except for a dramatic decrease of the T8+ cell fraction and an increase of the T10+ cell fraction. Functionally, the suppressor activity was completely lost, indicating a close correlation between phenotype and functional activity in this leukaemic cell population.

Adult↗
PubMed1985

Differential expression of HLA-DR antigens in subsets of human CFU-GM.

Expression of HLA-DR surface antigens by granulocyte/monocyte colony-forming cells (CFU-GM) may be important in the regulation of proliferation of these cells. Using immunological techniques to enrich for progenitor cells, we investigated the expression of HLA-DR in subsets of CFU-GM. "Early" (day 14) CFU-GM express higher levels of HLA-DR than do "late" (day 7) CFU-GM. Among late CFU-GM, cells destined to form monocyte (alpha-naphthyl acetate esterase-positive) colonies express higher levels of HLA-DR than do CFU-GM destined to form granulocyte (chloroacetate esterase-positive) colonies. Because high-level expression of DR antigen was a marker for monocyte differentiation, we examined several lymphokines for their effects on both DR expression and in vitro commitment to monocyte differentiation by myeloid precursor cells. DR antigen density could be increased by more than twofold over 48 hours upon exposure to gamma-interferon (gamma-IFN), whereas colony-stimulating factors had no effect. This was associated with a dose-dependent inhibition of total CFU-GM number, and a relative, but not absolute, increase in the ratio of monocyte colonies to granulocyte colonies. Similarly, in day 7 suspension cultures of purified myeloid precursor cells, gamma-IFN inhibited cell proliferation and increased the ratio of monocytes to granulocytes. Thus, despite the induction of high levels of HLA-DR antigen on precursor cells (a marker of monocyte commitment), the dominant in vitro effect of gamma-IFN was inhibition of granulocyte differentiation.

Antibodies, Monoclonal↗
PubMed1984

[Disorders of B cell activation in splenectomized patients].

Using a reverse hemolytic plaque assay as the effector system, we studied in vitro B-lymphocyte function in 12 patients after posttraumatic splenectomy as well as in 25 normal individuals. The time interval between the splenectomy and the immunological studies varied between 2 days and 7 years. Compared to normal individuals, the splenectomized patients had markedly elevated numbers of spontaneous immunoglobulin-secreting cells and severely decreased responses to the polyclonal activator pokeweed mitogen, indicating an in vivo polyclonal B-cell activation. A tendency towards normalization of these abnormalities, especially the high spontaneous ISC levels, could be observed during the time interval extending up to 7 years after splenectomy. In order to characterize the mechanism responsible for the altered immune response in splenectomized patients, in vitro experiments were performed with separated lymphocytes. These revealed an impaired T-helper cell capacity as well as an intrinsic B-cell defect. Marker analysis with monoclonal antibodies revealed normal proportions with the exception of OKT 4 positive and B 1 positive cells that identify T-helper/inducer and peripheral B-cells, respectively. We conclude that immune dysfunction in peripheral blood lymphocytes of splenectomized patients involves mainly the OKT 4 positive cell population.

Adult↗
PubMed1984

Ph1 positive blast crisis of chronic myeloid leukaemia exhibiting features characteristic of early T blasts.

Leukaemic cells from a patient in the blast crisis of chronic myeloid leukaemia were subjected to a surface marker analysis using a panel of monoclonal antibodies recognizing differentiation antigens of myeloid (MY7, MY906, VIM D5, M phi P9), erythroid (VIE G4), megakaryocyte (AN51), T-lymphoid (WT1, 10.2, OKT3, OKT4, OKT6, OKT8, OKT11A) and B-lymphoid cells (B1, B2, Y29/55), common ALL-antigen (VILA1), non-lineage-restricted antigens (OKT9, OKT10), monomorphic HLA-DR determinants (7.2) as well as TdT. When the patient entered his first blast crisis, his blasts expressed a phenotype corresponding to an immature myeloid cell (7.2+, MY7+, My906+, VIM D5-). Ph1-chromosome-positive blasts from this patient's first relapse had completely changed their surface marker characteristics: they had become TdT-positive and exhibited surface features characteristic of early T blasts (WT1+, 10.2+, OKT9+, OKT10+, 7.2-, OKT6-). Together, these features provide evidence that myeloid cells may share a common precursor with T cells.

Adult↗
PubMed1984

p69,71 antigen complex detected by monoclonal antibody Leu 1 in the identification of particular stages of malignant B-cell differentiation.

Lymphomatous cell samples from 86 patients with B-cell neoplasia (34 chronic lymphocytic leukaemia, 8 hairy-cell leukaemia, 5 prolymphocytic leukaemia, 20 immunocytic lymphoma, 9 centrocytic lymphoma, 3 centroblastic/centrocytic lymphoma, 3 lymphoblastic lymphoma, 1 plasma cell leukaemia and 3 plasmacytoma) were studied using the monoclonal antibody Leu 1, detecting a p69,71 antigen complex present on nearly all thymocytes, most (greater than 85%) peripheral T-lymphocytes as well as some malignant B-cells. Furthermore, we compared the reactivity of Leu 1-positive B-cells with those exhibiting conventional surface markers such as mouse-erythrocyte-receptor, FcIgG-receptor, C3b- or C3d-receptor and surface immunoglobulins of the various heavy- and light-chain types. Our results demonstrate a correlation between the expression of p69,71 antigen complex and distinct phenotypes revealed by conventional markers and underline the value of Leu 1 monoclonal antibody in the differential diagnosis of human B-cell neoplasia.

Antibodies, Monoclonal↗
PubMed1984

Abnormalities of B-cell activation and immunoregulation in patients with Crohn's disease.

We have studied B-lymphocyte function in 39 patients with Crohn's disease and 35 normal individuals using a reverse haemolytic plaque assay as the effector system. Ten patients had active Crohn's disease, the others being in an inactive state of the disease. Compared with normal individuals, the Crohn's disease patients - especially those in the active state of the disease - had markedly raised numbers of spontaneous immunoglobulin secreting cells and severely decreased responses to the polyclonal activator pokeweed mitogen. The differences between the reactivity of patients with active disease and those with inactive disease were statistically significant. These findings indicate an in vivo polyclonal B-cell activation in Crohn's disease patients, possibly due to antigen(s) or infectious agent(s). In vitro experiments were performed with separated lymphocytes in order to characterise the mechanism responsible for the altered immune reactivity in Crohn's disease. These revealed an intrinsic B-cell defect as well as an impaired T-helper cell capacity in patients with Crohn's disease. Findings supporting the hypothesis of an increased suppressor activity in Crohn's disease patients could not be observed, and marker analyses revealed normal proportions with the exception of raised Leu 7 positive cells that mediate 'natural killer' and 'killer' cytolysis. We conclude that immune dysfunction in peripheral blood lymphocytes of Crohn's disease patients involves B-cells as well as T-helper cells.

Adult↗
PubMed1984

T-ALL related to intermediate cortical/medullary thymocytes displaying functional and surface characteristics of suppressor T cells.

Leukemic cells of a patient with acute T-lymphoblastic leukemia (T-ALL) exhibiting the uncommon clinical feature of hypogammaglobulinemia were examined in terms of surface markers and immunologic functions. Employing various monoclonal reagents reacting with surface antigens present on T cells and additional conventional markers, it was shown that the patient's leukemic cells expressed a phenotypical profile (E-R+, TdT+, C3d-R-, OKT3-, T4-, T6(+), T 10+, T8++) corresponding to the intermediate stage between the cortical and medullary phase of normal thymocyte differentiation. Functionally, they were unable to respond to mitogens or to produce detectable amounts of immunoglobulins or to provide 'help' for allogeneic antibody production while they suppressed the immunoglobulin production of normal B cells by 76% in coculture experiments.

Adult↗
PubMed1984

Monoclonal antibodies recognizing T-cells (Leu 1) and transferrin receptor (OKT 9) crossreact with malignant B-cells of distinct differentiation stages.

The present study was carried out to determine the reactivity of Leu 1 and OKT 9 mouse monoclonal antibodies with B-cell samples obtained from 99 patients suffering from non-Hodgkin lymphomas of various B-type entities classified according to the Kiel-nomenclature. It could be demonstrated that both antibodies--previously known to display anti-T-cell reactivity--cross-react with several types of malignant B-cell. Leu 1 shows preference for membrane IgM and mouse erythrocyte receptor-bearing cells, whereas OKT 9 was expressed on malignant B-cells reflecting the terminal phase of B-cell ontogeny.

Antibodies, Monoclonal↗