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Biomedical subjects

E Klein

Publications and source records attributed to E Klein.

At least 307 records · Page 17Linked to original sources
PubMed1987

Effector or target cell selection mediated by C3 bridges.

Potential effector cells (including stimulated lymphocytes and cultured monocytes) and potential target cells of NK and AK type cytotoxic reactions (including several lymphoblastoid cell lines) cleave the third complement component (C3). As a result of expression of C3bA sites such cells are able to bind covalently the activated C3b through its metastable binding site and thereby become "armed" by the C3b. This permits C3b-bridge formation between these cells and CR1-bearing cells. The "effector selection" (i.e. when C3b is bound covalently to potential target cells) or "target selection" (when C3b is covalently bound to C3bA sites on potential effector cells) mediated by C3b bridges results in enhanced killing capacity. Macrophages activate and bind C3b as well; but the covalent binding of C3b by these cells inhibits Fc receptor mediated ADCC type killing.

Animals↗
PubMed1987

Quantitative comparison of direct and cold-target competition assay in monocyte- and complement-mediated lysis of sensitized erythrocytes.

Differences in the number of the antigenic determinants of A1 and B erythrocytes were exploited to study the influence of the sensitization on antibody-dependent monocyte- and complement-mediated cytotoxicity. Lysis was compared in direct and cold target competition assays. The findings were: (1) Monocyte mediated lysis of both targets was similar; A1 erythrocytes, however, showed stronger competitive inhibition than B cells; (2) the competitive inhibition was influenced by the antiserum concentration in a range where the direct lysis was not; (3) in the presence of optimal concentrations of hyperimmune antisera and complement, A1 erythrocytes were lysed, while B erythrocytes were not; and (4) A1 cells exposed to suboptimal concentrations of complement consumed complement, while B cells did not. It was concluded that the cold target competition assay is more sensitive than the direct cytotoxicity test to detect differences in the sensitization of erythrocytes.

Antibodies↗
PubMed1987

[Functional assessment, using micturition cystourethrography, of the unstable bladder in childhood].

The accuracy and reliability of a modified method of micturating urethrocystography for the diagnosis of uncontrolled detrusor contraction in unstable bladders (sphincter-detrusor dyssynergy during bladder filling) was studied in 100 patients aged between four and 15 years. A comparison with a urodynamic method showed an accuracy of 92%, sensitivity of 93% and specificity of 90.7%. The technique and indications are described and the clinical relevance of the results is discussed.

Adolescent↗
PubMed1987

Down-regulation of class I HLA antigens and of the Epstein-Barr virus-encoded latent membrane protein in Burkitt lymphoma lines.

Epstein-Barr virus (EBV)-carrying Burkitt lymphoma (BL) cells are relatively or completely resistant to the lytic effect of major histocompatibility complex class I HLA antigen-restricted cytotoxic T lymphocytes (CTLs) generated by stimulating lymphocytes of EBV-seropositive donors with the autologous EBV-transformed lymphoblastoid cell line (LCL). We previously found that EBV-negative and EBV-carrying BL lines derived from HLA-A11-positive donors were not only resistant to lysis by the HLA-A11-restricted CTL generated by stimulation with the autologous LCL, but also to HLA-A11-specific CTL derived from lymphocytes of an EBV-seronegative donor stimulated with an allogeneic LCL. Using the same and additional cell lines, we now show that the CTL resistance of the BL lines is probably due to a selective down-regulation of HLA-A11. We also show that the EBV-encoded latent membrane protein is expressed at a lower level in the EBV-carrying BL lines than in EBV-transformed LCLs. Only one of eight in vitro EBV-converted BL lines that shifted to a more LCL-like growth pattern expressed LMP at a high level. This line also reexpressed the HLA-A11 antigen that was undetectable in its EBV-negative progenitor. Our findings suggest that the typical BL cell phenotype is associated with low expression of both proteins.

Antigens, Neoplasm↗
PubMed1987

Endoscopic retrograde cholangiography in the detection of small stones in the gallbladder.

Multiple small (2-5 mm in size) gallstones were demonstrated only by endoscopic retrograde cholangiopancreatography in eight patients who had recurrent upper abdominal pain and vomiting. Three patients had mild, rapidly resolving abnormalities of liver biochemistry and serum amylase. In the other five, both serum amylase and liver biochemistry were repeatedly normal. We conclude that endoscopic retrograde cholangiography may be useful in the detection of small gallstones in patients with symptoms suggestive of biliary tract disease, even in the presence of normal oral cholecystography, ultrasonography, serum amylase, and liver biochemistry.

Amylases↗
PubMed1987

Mechanism of the potentiation of thrombolysis by pentoxifylline (Trental).

Streptokinase induced thrombolysis of radioactive labeled human fibrin clots was potentiated by simultaneous treatment with pentoxifylline (Trental). This appears to be due in part to the prevention of platelet aggregation on the clot. In addition, release of t-PA and PgI2 from the endothelium and increases in red cell deformability may also play a role.

Animals↗
PubMed1986

[Ciprofloxacin in Salmonella infection and abdominal typhoid].

Ten patients - two with Salmonella septicaemia associated with AIDS; one each Salmonella excretors in the convalescence stage and with Salmonella osteomyelitis; three with abdominal typhoid, and three with Salmonella enteritis - were treated with the gyrase inhibitor ciprofloxacin. The drug was given for 3-33 days, at a dosage of 250-750 mg orally in most cases. Clinical and bacteriological cure was achieved in nine patients. There were no significant side effects. One patient developed a macular rash, which is within the usual side-effect rate.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Radiation leukemia virus-transformed immunocompetent T cells. II. Antigen-induced macrophage migration inhibition factor and leukocyte migration inhibition factor production.

OVA-specific T cells were immortalized by infection with radiation leukemia virus (RadLV). Some clones derived from such population were shown to exhibit helper activity. We then tested clones without such function and found among them some that secreted macrophage migration inhibition factor (MIF) and leukocyte migration inhibition factor (LIF) upon exposure to the antigen in vitro. The lymphokine-producing clones, which were Thy-1+, Ly-1+ and Ly-2-, did not secrete MIF and LIF constitutively. Like other antigen-specific T cells, the immortalized clones could not be stimulated by free soluble antigen but required macrophages for presentation and for triggering the lymphokine production. The antigen-activated clones exclusively produced MIF and LIF, but not interleukin 2 or colony-stimulating factor. They neither provided helper activity nor induced delayed-type hypersensitivity. The data suggest that the T-cell clones carry the antigen receptors and that their antigen-inducible biological function is restricted to the migration inhibitory factor production.

Animals↗
PubMed1986

Lysis of autologous tumor cells by high-density lymphocytes is potentiated by the streptococcal preparation OK432 (Picibanil).

In experiments performed with tumor cells isolated from surgical specimens and lymphocytes collected at the time of surgery, tumor cells are often lysed by blood lymphocytes. Some of the effectors are present in the high-density T-cell subset. This population has little or no anti-K562 activity. For the auto-tumor lysis of T cells with high density, CD8-positive cells are mainly responsible. OK432 pretreatment of the effectors potentiates the existing lytic function or induces it in cases in which the cells have no such function. In general, the potentiating effect reflects inherent patterns of cytotoxicity. In contrast to the lysis of autologous tumor cells, cells with low but not high density were induced to lyse K562.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1986

Differential recognition of tumor-derived and in vitro Epstein-Barr virus-transformed B-cell lines by fetal calf serum-specific T4-positive cytotoxic T-lymphocyte clones.

Two interleukin-2 (IL-2)-dependent cytotoxic T-cell clones were obtained by limiting dilution from a lymphocyte culture stimulated in vitro with the autologous Epstein-Barr virus-transformed lymphoblastoid cell line (LCL) in the presence of fetal calf serum (FCS). Both clones uniformly had a T3+, T4+, Dr+ phenotype and lysed autologous B blasts, the autologous LCL, and allogeneic B cell lines sharing major histocompatibility complex (MHC) class II antigens. The cytotoxic function was triggered by FCS-derived components. There was no killing if the sensitive targets were cultured in serum-free medium or in medium supplemented with human serum. Sensitivity to lysis could be restored by exposing the targets to FCS for at least 6 hr at 37 degrees C. Monoclonal antibodies directed to T-cell-specific surface antigens and MHC class II antigens inhibited lysis with different efficiencies depending on the target cell origin. Killing of Burkitt's lymphoma (BL)-derived cell lines was blocked more easily than killing of LCLs. LCLs but not BL lines induced proliferation of the T-cell clones in the absence of exogenous IL-2. The differences were not related to quantitative variations in the expression of MHC class II antigens, indicating that BL lines differ from LCLs in other cell membrane properties that may influence antigen presentation. The results suggest that the affinity of effector/target binding, which is probably influenced by the concentration of antigenic determinants expressed on the target cell membrane, determines whether proliferative responses or cytotoxicity are induced in the antigen-recognizing T cells.

Antibodies, Monoclonal↗
PubMed1986

B cell activation by the nontransforming P3HR-1 substrain of the Epstein-Barr virus (EBV).

The P3HR-1 substrain of Epstein-Barr virus does not transform B cells. This defect is known to be determined by the loss of the coding sequence for the nuclear antigen EBNA-2. The virus can attach to and enter resting B cells. The initial events after EBV infection are reminiscent of those induced by polyclonal B cell activators. Similar to the effect of these, P3HR-1 virus lowers membrane IgD expression on B cells and abrogates the transient elevation of activation markers BB-1 and LB-1 induced by the culture conditions. An important event of B cell activation is the acquisition of competence to respond to specific growth factors produced by T cells. This was induced by the P3HR-1 virus. The infected B cells had elevated [3H]thymidine incorporation when exposed to the supernatant of PHA-treated T cells. The EBV receptor is identical with the complement receptor CR2. Ligand binding to CR2 has been shown both with mouse and human B cells to deliver certain activation signals. Therefore, it is possible that the early step of activation by EBV is initiated through the binding to the receptor and is thus a cell surface event.

Antigens, Surface↗
PubMed1986

Lysis of autologous tumor cells by blood lymphocytes tested at the time of surgery. Correlation with the postsurgical clinical course.

Lymphocyte-mediated lysis of autologous tumor cells (autologous lymphocyte cytotoxicity ALC) was tested at the time of surgery in 108 patients (46 squamous cell carcinomas of the lung, 25 adenocarcinomas of the lung, 19 soft tissue sarcomas and 18 osteosarcomas). The clinical course of these patients in relation to the test results has been published previously. The group was evaluated again after an extended observation time, now with a mean of 80.2 months (range 36-108). The test was rarely positive in patients with metastasis (2 out of 28 experiments). There was a correlation between the ALC results and the postsurgical clinical course for patients without detectable metastasis in that (1) a negative test was invariably a bad prognostic sign, i.e., all 32 patients with negative ALC died within 3 years (mean survival time 16.1 months). (2) The remission and survival times were longer for the ALC positive patients (p less than 0.001). (3) All 37 individuals who are alive at present without recurrence belong to the reactive group. The ALC results correlated with the clinical course in 88% of patients. The correlation was highest for the groups of soft tissue sarcoma and adenocarcinoma of the lung. There was no correlation between killing of K562 cells and ALC, or between lymphoproliferative response to PHA and ALC reactivity.

Adenocarcinoma↗