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M Linker-Israeli

Publications and source records attributed to M Linker-Israeli.

54 records · Page 3Linked to original sources
PubMed1985

Correction of interleukin-2 production in patients with systemic lupus erythematosus by removal of spontaneously activated suppressor cells.

Interleukin-2 (IL-2) production in vitro is depressed in systemic lupus erythematosus (SLE) patients. It is not known whether this abnormality is caused by a defect in the producer lymphocytes or by excessive suppression. We report that removal of OKT8 (Leu 2a)+ cells increased the IL-2 production by in vitro-stimulated lymphocytes to normal or above normal levels in 19 of 21 SLE patients. This increase was more apparent in those patients with clinically inactive disease and/or receiving less than 7.5 mg of prednisone. Removal of OKT8+ cells from normals did not significantly increase IL-2 activity. SLE, but not normal, OKT8+ cells decreased IL-2 production when added back to autologous OKT8-depleted cells. In some experiments, OKT8+ cells from normal donors also suppressed IL-2 production in SLE. This result suggests that the defect in IL-2 production is complex and may involve multiple cell interactions. Three lines of evidence suggest that the SLE OKT8+ cells actively inhibit the production of IL-2 rather than passively absorb this lymphokine: (a) only 3.2% of SLE lymphocytes expressed IL-2 receptors as detected with anti-Tac; (b) freshly prepared SLE lymphocytes did not absorb IL-2; and (c) cell-free supernatants from SLE OKT8+ cells inhibited IL-2 production, but not IL-2 activity. Double-labeling studies by flow cytometry revealed that 19.3% of SLE OKT8+ cells were also Ia-positive, and approximately 33% co-expressed the natural killer cell marker, HNK-1 (Leu 7). Removal of Leu 7+ cells also significantly elevated IL-2 production in SLE. These studies suggest that one or more circulating mononuclear cell subsets in SLE patients can suppress IL-2 production and that one subset may possibly belong to a non-T, non-B "third mononuclear population."

Adult↗
PubMed1983

Defective production of interleukin 1 and interleukin 2 in patients with systemic lupus erythematosus (SLE).

The objective of this study was to define some causes of the immunologic impairment characteristic of systemic lupus erythematosus. Blood mononuclear cells from 19 patients were stimulated to produce interleukin 1 and interleukin 2 and compared with controls. A severe defect in both IL 1 and IL 2 activity was observed. The low cytokine levels did not correlate with clinical or serologic activity of disease. These defects could not be explained by concurrent corticosteroid therapy. There was no correlation between a lower number of OKT4+ cells observed in these patients and the levels of IL 2 production, nor did removal of monocytes bring IL 2 to normal. Impaired IL 2 production could not be restored to normal by IL 1. The observed deficiency in these regulatory cytokines may therefore be a primary defect that is important in the pathogenesis of this disorder.

Animals↗
PubMed1982

The immunological classification of leukaemia based on a rapid microcytotoxicity test.

We describe a rapid, accurate, and reproducible cytotoxic antibody test for the immunological classification of leukaemia. Well characterized heteroantisera and monoclonal antibodies were distributed in a microcytotoxicity tray referred to as a leukaemia screening tray (LST). Leukaemia cells were tested for the presence of Ia-like, 'blast', thymocyte, common acute lymphoblastic leukaemia (cALL), and acute myeloblastic leukaemia (AML) antigens. Utilizing this technique, T ALL could be distinguished from non-T ALL, ALL and AML could be differentiated, the myeloid blast crisis of chronic myelogenous leukaemia (CML) could be distinguished from the lymphoid blast crisis, and the T lymphocyte and B lymphocyte lymphoid leukaemias were readily identified. It has been shown that subclassification of leukaemia according to surface markers, as described here, offers considerable improvement in the diagnosis and treatment of leukaemia over the classical morphological methodologies. Because the test can be completed in 2 hr and unlimited amounts of monoclonal antibodies are available, the LST or similar tests should become universally available in the future to supplement morphological data and replace other lengthy enzyme and rosetting tests.

Antibodies, Monoclonal↗
PubMed1981

Monoclonal antibodies reactive with acute myelogenous leukemia cells.

Two cytotoxic monoclonal antibodies (D5D6 and C10H5) were raised to acute myelogenous leukemia (AML) cells. One of them, D5D6, reacted with 100% of the cells from 44/50 AML patients. The second, C10H5, reacted with 100% of the cells from 13/39 AML patients. D5D6 and C10H5 were cytotoxic to 100% of the monocytes from all healthy donors tested. Apart from monocytes, these antibodies did not react with any other peripheral blood cells from normal donors or with cancerous cells either from cell culture lines or from patients with chronic myelogenous leukemia (CML), lymphoid leukemias, or solid tumors. These antibodies inhibited the growth of the myeloid-monocytic stem cell, the CFU-C, and reacted with a minor population of normal bone marrow cells by immunofluorescence. Both D5D6 and CH5 have potential utility for the differential diagnosis of acute leukemia, for the detection of early leukemic relapse, and for enrichment of human stem cells.

Animals↗
PubMed1980

Serum antibodies to human fetal antigens in patients with systemic lupus erythematosus (SLE).

Serum antibodies to human fetal antigens were measured by a radiolabeled anti-immunoglobulin binding assay by using human fetal fibroblasts (Flow cell line No. 1000) as target cells. High titers of IgG antibody to the fetal cells were found in sera of patients with systemic lupus erythematosus (SLE). The antibody reacted with surface membrane antigens shared by various fetal tissues of human and murine origin but not by adult tissues. The reaction of the SLE antibody to the fetal cells was inhibited by heterologous antiserum to the Flow 1000 cells and antiserum to murine embryonic fibroblasts, but not by antiserum to human alpha-fetoprotein or human fibronectin. Absorption of SLE serum with isolated nuclei did not abolish the reaction indicating that these were not anti-nuclear antibodies. The antibody activity was found to reside in the F(ab')2 fragment. The serum titer of the anti-fetal antibody was higher in SLE patients with active disease than those in clinical remission.

Animals↗
PubMed1977

Cell surface components of carcinogen-induced lymphoid tumors in SJL/J mice.

Preleukemic cells could be detected in the bone marrow cell population of SJL/J mice within several days after induction of leukemia by repeated feedings with a chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Bone marrow cells collected 7, 30 or 60 days following carcinogenic treatment, developed lymphoid tumors upon transplantation into syngeneic irradiated recipients. The incidence of these tumors varied between 40--45% when the bone marrow cells were collected and transferred 7--30 days after feeding with DMBA, and raised to an incidence of 80% when transferred 60 days after carcinogen administration (compared to 50% incidence in the DMBA-treated bone marrow donors). A survey of several cell surface components on the lymphoid tumor cells, obtained after transplantation of preleukemic cells, indicated that most of the tumor lines bore both the Thy-1.2 antigen (weak) and the Fc receptor, whereas the rest were positive only for the Fc receptor. None of these tumor cell lines would yield a significant amount of cell-bound immunoglobulin.

9,10-Dimethyl-1,2-benzanthracene↗