Increased bactericidal activity by non-specific stimulation of lymphoid cells—Experiments in vivo with Concanavalin A

1973 ◽  
Vol 2 (1) ◽  
pp. 74-81 ◽  
Author(s):  
Frederick C. Lane ◽  
Jean Claude Petit ◽  
Ethel Gordon ◽  
Emil R. Unanue
Keyword(s):  
Concanavalin A ◽  
Bactericidal Activity ◽  
Lymphoid Cells ◽  
Specific Stimulation ◽  
Stimulation Of

Specific stimulation of heart sarcolemmal Ca2+Mg2+ ATPase by concanavalin A

1989 ◽  
Vol 268 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Dayuan Zhao ◽  
Naoki Makino ◽  
Naranjan S. Dhalla
Keyword(s):  
Concanavalin A ◽  
Specific Stimulation ◽  
Stimulation Of

scholarly journals The role of calcium ions in the regulation of rat thymocyte pyruvate oxidation by mitogens

1978 ◽  
Vol 174 (3) ◽  
pp. 711-716 ◽  
Author(s):  
D A Hume ◽  
E K Vijayakumar ◽  
F Schweinberger ◽  
L M Russell ◽  
M J Weidemann
Keyword(s):  
Concanavalin A ◽  
Metabolic Response ◽  
Ionophore A23187 ◽  
Complete Metabolic Response ◽  
Isolated Mitochondria ◽  
Pyruvate Oxidation ◽  
Specific Stimulation ◽  
Nanomolar Range ◽  
Stimulation Of

1. Calcium concentrations in the nanomolar range cause a specific stimulation of the oxidation of pyruvate by isolated mitochondria from rat thymus that is sufficient to account precisely for the stimulation of pyruvate oxidation observed when rat thymocytes are incubated with the mitogens concanavalin A or ionophore A23187. 2. Higher concentrations of Ca2+ (more than 50 nM) inhibit the oxidation of NAD+-linked substrates by rat thymus mitochondria without affecting the oxidation of succinate or ascorbate+ NNN′N′-tetramethyl-p-phenylendiamine. 3. The addition of Ni2+ or Co2+ (2mM) to rat thymocytes prevents the response to concanavalin A at the level of pyruvate oxidation without affecting the stimulation of glycolysis induced by this mitogen. In contrast, the complete metabolic response to the ionophore A23187 is abolished by these ions. Ni2+ and Co2+ interfere with the ability of the ionophore to transport Ca2+ across the plasma membrane. 4. Concanavalin A, but not ionophore A23187, increases the respiratory inhibition induced by Ni2+ and Co2+. 5. These results support the view that mitogens stimulate lymphocyte pyruvate oxidation through an increase in cellular Ca2+ uptake.

Stimulation of in vivo antibody production and concanavalin-A-induced mouse spleen cell mitogenesis by prolactin

1987 ◽  
Vol 14 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Bryan L. Spangelo ◽  
Nicholas R.S. Hall ◽  
Philip C. Ross ◽  
Allan L. Goldstein
Keyword(s):  
Spleen Cell ◽  
Antibody Production ◽  
Concanavalin A ◽  
Mouse Spleen ◽  
Mouse Spleen Cell ◽  
Stimulation Of

scholarly journals IN VITRO STUDIES ON RADIATION LYMPHOID RECOVERY OF MOUSE SPLEEN

1966 ◽  
Vol 123 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Amiela Globerson
Keyword(s):  
Bone Marrow ◽  
Organ Culture ◽  
Culture Method ◽  
Lymphoid Cells ◽  
In Vitro Studies ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Stimulation Of

In vitro studies, utilizing an organ culture method were reported on mutual interactions between irradiated spleen, normal bone marrow, and thymus. It has been shown; (a) that singly isolated spleen explants were incapable of lymphoid regeneration, (b) thymus had no stimulatory effect on spleen regeneration, (c) bone marrow interacted synergistically with spleen leading to appearance of lymphoid cells which were not detected in singly isolated bone marrow or spleen, and (d) no stimulation of lymphopoiesis in bone marrow was conferred by thymus in the absence of spleen. The results are discussed in terms of possible mechanisms involved in lymphoid radiation recovery in vivo.

scholarly journals THE INFLUENCE OF IMMUNOLOGICALLY COMMITTED LYMPHOID CELLS ON MACROPHAGE ACTIVITY IN VIVO

1969 ◽  
Vol 129 (5) ◽  
pp. 973-992 ◽  
Author(s):  
G. B. Mackaness
Keyword(s):  
Specific Interaction ◽  
Acquired Resistance ◽  
Peritoneal Macrophages ◽  
Lymphoid Cells ◽  
Delayed Type Hypersensitivity ◽  
Activated Macrophages ◽  
Macrophage Activity ◽  
Cytophilic Antibody ◽  
Stimulation Of

It has been shown that the immune response of mice to infection with L. monocytogenes gives rise to a population of immunologically committed lymphoid cells which have the capacity to confer protection and a proportionate level of delayed-type hypersensitivity upon normal recipients. The cells were most numerous in the spleen on the 6th or 7th day of infection, but persisted for at least 20 days. Further study revealed that the immune cells must be alive in order to confer protection, and free to multiply in the tissues of the recipient if they are to provide maximum resistance to a challenge infection. The antibacterial resistance conferred with immune lymphoid cells is not due to antibacterial antibody; it is mediated indirectly through the macrophages of the recipient. These become activated by a process which appears to depend upon some form of specific interaction between the immune lymphoid cells and the infecting organism. This was deduced from the finding that immune lymphoid cells from BCG-immunized donors, which were highly but nonspecifically resistant to Listeria, failed to protect normal recipients against a Listeria challenge unless the recipients were also injected with an eliciting dose of BCG. The peritoneal macrophages of animals so treated developed the morphology and microbicidal features of activated macrophages. It is inferred that acquired resistance depends upon the activation of host macrophages through a product resulting from specific interaction between sensitized lymphoid cells and the organism or or its antigenic products. Discussion is also made of the possibility that activation of macrophages could be dependent upon antigenic stimulation of macrophages sensitized by a cytophilic antibody.

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