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Molecular magnesium hydride with a terminal metal-hydrogen bond [Mg(iPr2TACN·AliBu3)H]2 supported by a monoanionic TACN-type ligand (TACN = 1,4-di-isopropyl-1,4,7-triazacyclononane) rearranges to form the dinuclear magnesium hydride [Mg(iPr2TACN·AlHiBu2)(µ-H)]2, exhibiting a rare MgH-Al interaction.

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The supernatant of mitogen- or antigen-stimulated mononuclear cell cultures is known to contain a large number of biologically active molecules. In the present study, we have stimulated human mononuclear cells and rat spleen cells with Con A or antigen (PPD) respectively to produce lymphokines, such as histamine releasing factor (HRF), which is capable of causing histamine release from rat mast cells and human basophils. Histamine was measured fluorimetrically by Shore et al. This assay is sensitive and reproducible: replicates varied by less than 15% in triplicate samples.

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In 43 recipients of allogenic cadaver kidneys before and three times a week after transplantation to the discharge from the hospital care the antibody titre against the Thomsen-Friedenreich-antigen (Anti-T) was determined and the score value was calculated from the agglutination intensity. A prognostic significance of the value got before operation could not be found. No changes of the titre appeared under the influence of the postoperatively performed immunosuppression as well as in connection with rejection crises. In 9 patients with clinically manifest systemic infections (8 cytomegalovirus infections, 1 bacterial infection) unequivocal (greater than or equal to 8 fold) increases of the anti-T-titre could be proved. These findings speak for an infection-induced formation of these cross-reacting anti-T-antibodies.

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The combined application of psoralen and UVA radiation to skin grafts induced a prolongation of the survival time of the grafts in mice. This was observed using the H-Y barrier, an allogeneic barrier without H-2 disparities, and a strong H-2 incompatible barrier. The effect is probably due to a reduction of antigen-presenting cells, or to other, unknown mechanisms.

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Histamine inhibits the chemiluminescence response of human lymphocytes to Concanavalin A by interfering with early triggering events. The inhibition seems to be mediated via H2 receptors, acts immediately, and is reversible by washing. A longer incubation in a histamine-containing medium induces a refractory state of the cells. The inhibitory effect described here is compared with the inhibitory action of histamine in the lymphocyte transformation test.

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2-Cyanoethylurea (2; CEU or BA 1-4) obtainable from 1-carboxamido-2-cyanoaziridine (2; BA l) by ring fission possesses immunomodulating properties like its parent compound containing the intact aziridine ring, as well as other 2-cyanoaziridine (1) derivatives. As was shown in a mouse model, CEU accelerated the time of rejection of skin allografts (immunostimulation) and reduced the prolonged tolerance time of mice immunosuppressed with cyclophosphamide to values found in normal control animals (immunorestoration).

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Three substances known to act on N-acetylneuraminic acid (NANA), were tested for their activity on rat peritoneal mast cells. Both neuraminidase, which splits off NANA, and the lectin from Cepaea nemoralis directed against NANA are histamine releasers. Periodate itself did not trigger the cells but inhibited the releasing action of other substances. The results provide further evidence for the role of NANA in the triggering of mast cells. A cytotoxic substance, benzyl-polyethylene imine, triggers mast cells without affecting NANA. In addition, the role of histamine-BSA conjugates as histamine releasers is described.

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The histamine binding capacity of cells in various lymphoid organs has been determined by flow cytofluorometric (FCF) analysis of histamine receptors. Using fluoresceinated bovine serum albumin conjugated to histamine (HIS-BSA-FITC) as a staining reagent two distinct lymphocyte subpopulations of differing fluorescence intensity have been identified in each organ investigated. The thymus has a low number of histamine-receptor bearing cells, while bone marrow, lymph nodes and spleen reveal increasing binding capacities to the histamine conjugate. It is suggested that there exists a different susceptibility of distinct lymphocyte subpopulations for histamine, thereby enabling its controlled immunoregulatory activity.

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A rosetting of isolated rat mast cells with complement coated zymosan does not induce a histamine release. However, this procedure potentiated the release induced by ATP. Treatment of rats with prednisolone diminishes the number of the rosette forming mast cells.

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One of the two lectins, occurring in the albumen gland of the snail, Cepaea nemoralis L., is shown to be a histamine releaser from isolated rat mast cells as well as in vivo. The release reaction is induced in the same dosage range as the agglutination of human red blood cells occurs. Both the reactions are inhibitable by the addition of N-acetyl-neuraminic acid. The releasing activity of the lectin seems to be a counterpart to the triggering action of polycations, because its specificity is directed against this sugar.

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Literature review. Mast cells and basophils are included not only in anaphylactic but also in complement activating and cell-mediated immune reactions. A histamine release can be induced via the IgE mechanism, the anaphylatoxins, the histamine releasing activity, and by other reactions. Histamine and several other mediators induce a local inflammation reaction either by a direct action on their target cells or indirectly by the activation of other humoral and/or cellular effector systems. Histamine influences several immune reactions. Here, its influence on histamine receptor-bearing lymphocytes is discussed more in detail. Using in vitro test systems, it has been shown that histamine has a dual effect, it induces a suppression when applied in higher concentrations, while low concentrations are stimulating. In vivo, histamine receptor-bearing lymphocytes have suppressive functions, mediated by H2 receptors. Some preliminary evidence for the inclusion on histamine in the immunoreagulation of patients with several diseases is presented.

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The protamine sulfate-induced release of histamine from mast cells in a non-cytotoxic reaction, similar to the 48/80-induced secretion. Polyethylene imine was found to be a less potent releaser. It is a cytotoxic substance without specificity for mast cells and acts on membranes generally. Although the two agents are related concerning their molecular weight and polybasicity, their mode of action on mast cells is clearly different.

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Protamine sulfate, known for a long time as a histamine releaser, was labeled with a fluorescent dye (FITC). This conjugate was shown to stain selectively the mast cell fraction of rat peritoneal cells. Within a few seconds, the protamine was found inside the cells. Although the cells had lost their histamine completely, no granules were found outside the cells. In the electron microscope, the protamine treated mast cells showed a loss of the electron density of their granules, a vacuolization, and other signs of histamine release. Evidence for a direct connection between the vacuoles and the extracellular fluid was gained by incubating mast cells in FITC-labeled human serum albumin followed by the addition of unlabeled protamine. After washing, the fluorescence was found to be located inside the cells, demonstrating an influx of the FITC-HSA under the influence of protamine. The protamine-induced release reaction is increased after addition of Ca2+, reduced by lowering the temperature, addition of 2-deoxyglucose, or cytochalasin B. Disodium cromoglycate also diminished the histamine release in a dose dependent manner. Protamine did not induce a loss of lactate dehydrogenase from the mast cells. The release reaction is mediated by the cell membrane, as shown by the releasing activity of insolubilized protamine. We conclude that the protamine-induced release is a non-cytotoxic reaction, fulfilling some criteria of the anaphylactic histamine release.

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Using rat complement-treated zymosan particles a rosetting of purified rat peritoneal mast cells could be demonstrated. The question was investigated whether the binding of activated complement could be a trigger of histamine release. Varying the degree of complement label on the zymosan particles, the time and temperature of incubation and the dependence on Ca2+ ions, we could not induce a release of histamine in any case. The addition of labeled zymosan increased slightly the mediator release induced by ATP. The immunologic significance of the complement receptors on mast cells is still unclear.

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Using fluoresceine isothiocyanate labeled protamine sulfate it is possible to stain rat mast cell fractions of isolated periotoneal cells in a selective way. The cells are not degranulated, though they have lost their histamine completely. The method shows the dissociation of the mediator release and the extrusion of the granules.

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