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Electrophoretic analysis of the serum from a patient Im suffering from a multiple myeloma revealed the existence of two abnormal bands. Purification of these two fractions on a DEAE-cellulose column showed that both fractions had the same sedimentation coefficient (7S), belonged to the same class (IgG), and subclass (γ1) and bore the same allotype (Gm1). However, the heavy, (H) chains of one immunoglobulin were associated with type κ light (L) chains whereas those of the other were associated with type λ L chains. Three individual antigenic determinants were found in these two proteins. One was common to the H chains of both proteins and the other two were each specific to one of the L chains. These results suggest that the myeloma cells of patient (Im) were able to produce at least three polypeptide chains, one H chain and two different types of L chains. [ABSTRACT FROM AUTHOR]

The influence of the platelet-activating factor (PAF) antagonist, BN 52021, on human natural killer (NK) cell cytotoxicity against K 562 target cells was determined. Cytotoxicity was measured by a short-term (4 hr) 51Cr-release assay. The cytotoxicity was significantly reduced in the presence of PAF antagonist at concentrations from 30 to 120 μM. This reduction of killing was not due to the impairment of binding of effector cells to target cells. Pretreatment of K 562 target cells with the PAF antagonist led to a greater inhibition of NK cell cytotoxicity compared with that observed when the effector cells were preincubated with BN 52021. Thus, the inhibition of cytotoxicity appears to be due to an effect of BN 52021 on target cells rather than on lymphocytes. Furthermore, the increase in NK activity induced by interferon was less pronounced when BN 52021 was added in the incubation medium. The natural cytotoxicity of platelet-depleted or large granular lymphocyte-enriched effector cell populations was inhibited by the PAF antagonist in a similar manner. The effect of BN 52021 appears to be related to its specific PAF antagonistic activity since a similar action on NK cells was noted with two other structurally unrelated PAF antagonists, BN 52111 and WEB 2086. In contrast, Ginkgolide J (BN 52024), which is structurally related to BN 52021 but lacks PAF antagonistic activity, was ineffective in inhibiting NK cell cytotoxicity. Finally, synthetic PAF induces a dose-dependent cytotoxic action on K 562 cells and this effect of the autacoid is inhibited by BN 52021. These observations provide indirect evidence that PAF could play a role in the mechanism(s) of NK cytotoxicity. [ABSTRACT FROM AUTHOR]

Interleukin-9 (IL-9) is a mouse T-cell-derived cytokine that supports the growth of mucosal type mast cells suggesting its role in the regulation of type I hypersensitivity reactions. Therefore the possible effect of IL-9 on the in vitro regulation of IL-4-induced IgE and IgG1 releases in the mouse was investigated. In this report, we present evidence that IL-9 potentiated IL-4-induced IgE and IgG1 releases from lipopolysaccharide (LPS)-primed murine B lymphocytes, whereas IL-9 alone was ineffective. The potentiating effect of IL-9 is specific for IgE and IgG1 since no effect on IgM production was observed. This potentiating effect was neither related to an enhanced cell viability, nor to an alteration of the IL-4-induced expression of class II antigens by murine B cells. Besides the fact that IL-9 increased the number of IgG1-secreting cells, this cytokine might also enhance immunoglobulin release on a cell basis. Taken together, these data suggest that IL-9 plays an in vitro regulatory role in antibody synthesis, probably via a direct action on murine B lymphocytes.

Immune complexes (ICs) triggered the degranulation of basophils/mastocytes in rabbit and man, thus releasing histamine and platelet-activating-factor. ICs acted upon basophils/mastocytes through complement activation and generation of anaphylatoxins and through release of cationic proteins from polymorphonuclear neutrophils. Anaphylatoxins and cationic proteins were active on human and rabbit mastocytes and on human basophils but not on rabbit basophils. Therefore, a cascade of cell to cell interactions may be envisaged implicating successively neutrophils, basophils and/or mastocytes and platelets. These interactions result in enhanced vascular permeability that allows ICs to be trapped along filtering basement membranes. This sequence could perpetuate the deposition of ICs, initially triggered by degranulation of basophils and mastocytes through the IgE-dependent mechanism, and furnish us with an explanation for the rather poorly understood involvement of platelets in immunopathology.