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  • 1
    Publication Date: 1980-04-01
    Description: A human homogeneous IgM/K cold agglutinin (CA) Sa is described, whose corresponding antigen on erythrocytes (RBC) was abolished by neuraminidase. This indicated that the antigen was related to N- acetylneuraminic acid, similar to Pr and Gd antigens. In contrast, this antigen was only partially destroyed by proteases, whereas Pr antigens are completely destroyed and Gd antigens are not influenced by proteases. Sa antibody activity was inhibited by sialyllactose NeuAc (alpha 2 leads to 3) (alpha 2 leads to 6) Gal (beta, 1 leads to 4) Glc like anti-Gd but in contrast to anti-Pr. The corresponding antigen was associated with an RBC membrane glycoprotein fraction like Pr, Sa is one of a spectrum of human monoclonal CA against cell surface neuraminyl groups.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 2
    Publication Date: 1980-04-01
    Description: A human homogeneous IgM/K cold agglutinin (CA) Sa is described, whose corresponding antigen on erythrocytes (RBC) was abolished by neuraminidase. This indicated that the antigen was related to N- acetylneuraminic acid, similar to Pr and Gd antigens. In contrast, this antigen was only partially destroyed by proteases, whereas Pr antigens are completely destroyed and Gd antigens are not influenced by proteases. Sa antibody activity was inhibited by sialyllactose NeuAc (alpha 2 leads to 3) (alpha 2 leads to 6) Gal (beta, 1 leads to 4) Glc like anti-Gd but in contrast to anti-Pr. The corresponding antigen was associated with an RBC membrane glycoprotein fraction like Pr, Sa is one of a spectrum of human monoclonal CA against cell surface neuraminyl groups.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Location Call Number Expected Availability
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  • 3
    Publication Date: 1986-02-01
    Description: The present studies were designed to investigate the mechanism(s) of the defective T cell proliferative response to various stimuli in patients with B cell chronic lymphocytic leukemia B-CLL. In 14 patients with advanced B-CLL (stage III or IV) we found the T cell response in the autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR) to be 35.7% and 30% of the controls, respectively. Proliferation in the MLR depends upon the production of and response to interleukin 2 (IL 2), a T cell growth factor. IL 2 production in eight B-CLL patients was 22% of the control. The response to IL 2 was measured by the increase in the T cell proliferation in the MLR with the addition of IL 2. T cell proliferation in both the auto and allo MLR of CLL patients was significantly lower than in the controls after the addition of IL 2. The proliferative response of normal T cells to stimulation by CLL B cells was 50% of the control. This latter response was increased to control levels when cultures were supplemented with exogenous IL 2, suggesting that CLL B cells could stimulate IL 2 receptor generation in normal T cells in an allo MLR, but not IL 2 production. The presence of IL 2 receptors on activated T cells was directly determined using anti- Tac, a monoclonal antibody with specificity for the IL 2 receptor. Of the mitogen- or MLR-activated T cells in CLL patients, 6% and 10%, respectively, expressed Tac antigen, whereas identically stimulated control T cells were 60% and 47% Tac+, respectively. Our findings suggest that T cells in B-CLL are defective in their recognition of self or foreign major histocompatibility antigens as demonstrated by their impaired responsiveness in the MLR. Thus, these cells are unable to produce IL 2 or generate IL 2 receptors.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 4
    Publication Date: 1986-02-01
    Description: The present studies were designed to investigate the mechanism(s) of the defective T cell proliferative response to various stimuli in patients with B cell chronic lymphocytic leukemia B-CLL. In 14 patients with advanced B-CLL (stage III or IV) we found the T cell response in the autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR) to be 35.7% and 30% of the controls, respectively. Proliferation in the MLR depends upon the production of and response to interleukin 2 (IL 2), a T cell growth factor. IL 2 production in eight B-CLL patients was 22% of the control. The response to IL 2 was measured by the increase in the T cell proliferation in the MLR with the addition of IL 2. T cell proliferation in both the auto and allo MLR of CLL patients was significantly lower than in the controls after the addition of IL 2. The proliferative response of normal T cells to stimulation by CLL B cells was 50% of the control. This latter response was increased to control levels when cultures were supplemented with exogenous IL 2, suggesting that CLL B cells could stimulate IL 2 receptor generation in normal T cells in an allo MLR, but not IL 2 production. The presence of IL 2 receptors on activated T cells was directly determined using anti- Tac, a monoclonal antibody with specificity for the IL 2 receptor. Of the mitogen- or MLR-activated T cells in CLL patients, 6% and 10%, respectively, expressed Tac antigen, whereas identically stimulated control T cells were 60% and 47% Tac+, respectively. Our findings suggest that T cells in B-CLL are defective in their recognition of self or foreign major histocompatibility antigens as demonstrated by their impaired responsiveness in the MLR. Thus, these cells are unable to produce IL 2 or generate IL 2 receptors.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Location Call Number Expected Availability
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