Search results for: Mouse Anti-Human B2M Antibodies
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CXCR4 regulates migration and development of human acute myelogenous leukemia stem cells in transplanted NOD/SCID mice.
The chemokine stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 participate in the retention of normal hematopoietic stem cells within the bone marrow (BM) and their release into the circulation. Homing and engraftment of human stem cells in immunodeficient mice are dependent on cell surface CXCR4 expression and the production of BM SDF-1, which acts also as a survival factor for both human and murine stem cells. However, the role of SDF-1/CXCR4 interactions in the control of human acute myelogenous leukemia (AML) cell trafficking and disease progression is poorly understood. In this study, we report that although some AML cells do not express surface CXCR4, all AML cells tested express internal CXCR4 and SDF-1. Culture of AML cells with SDF-1 promoted their survival, whereas addition of neutralizing CXCR4 antibodies, SDF-1 antibodies, or AMD3100 significantly decreased it. Pretreatment of primary human AML cells with neutralizing CXCR4 antibodies blocked their homing into the BM and spleen of transplanted NOD/SCID/B2m(null) mice. Furthermore, weekly administrations of antihuman CXCR4 to mice previously engrafted with primary AML cells led to a dramatic decrease in the levels of human AML cells in the BM, blood, and spleen in a dose- and time-dependent manner. Interestingly, the same treatment did not affect significantly the levels of normal human progenitors engrafted into NOD/SCID mice. Taken together, our findings demonstrated the importance of the SDF-1/CXCR4 axis in the regulation of in vivo motility and development of human AML stem cells and identified CXCR4 neutralization as a potential treatment for AML.Sigal Tavor, Isabelle Petit, Svetlana Porozov, Abraham Avigdor, Ayelet Dar, Leonor Leider-Trejo, Noga Shemtov, Varda Deutsch, Ella Naparstek, Arnon Nagler, Tsvee Lapidot
1584 related Products with: CXCR4 regulates migration and development of human acute myelogenous leukemia stem cells in transplanted NOD/SCID mice.
1 mg10 ug1.00 flask1.00 flask5ug1.00 flask11mg1.00 flask1 mg1.00 flask100 μg
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The role of macrophages in stimulation of immune induction and myelopoiesis. I: Comparison of activity of macrophage-derived factors in granulopoiesis and immunostimulation.
Hemopoietic growth and immunological inductive factors from human peripheral leukocyte conditioned medium and mouse macrophage culture supernatant fluids were compared. Factors derived from human peripheral leukocyte conditioned medium were found to substitute for those of mouse macrophage derivation in immunological assays, namely, induction of a cytotoxic T-lymphocyte response in macrophage-depleted mouse spleen cultures. Association of macrophage-derived factors with B2-microglobulin (B2m) antigen determinants was observed by inhibition with great antihuman B2m, affinity chromatography, and direct replacement of mouse macrophage-derived factors with human urinary B2m.G B Price, R M Gorczynski
1948 related Products with: The role of macrophages in stimulation of immune induction and myelopoiesis. I: Comparison of activity of macrophage-derived factors in granulopoiesis and immunostimulation.
5 G5ug48 assays 2ug96T2ug400Tests
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Inhibition by anti-beta2-microglobulin antisera of responder cells and not of stimulator cells in the mixed lymphocyte reaction.
Specific antisera directed against beta2-microglobulin (B2m) have been shown to inhibit completely the mixed lymphocyte reaction (MLR). However, the mechanism of inhibition has been unclear. In the present study, further experiments were performed to determine the effect of anti-B2m on both the stimulator and responder cells in an MLR. The experimental design used was that of a xenogeneic MLR, using mouse and human lymphocytes. The ffect of anti-human B2m was studied in this system. Anti-human B2m inhibited the xenogeneic MLR only when human lymphocytes were used as responder cells and did not inhibit the MLR when they were used as stimulator cells...R T McCalmon, R T Kubo, H M Grey