Annales d'immunologie最新文献

This study was performed on four sibling pairs affected by cystic fibrosis. Of each sibling pair, one was more affected than the other. The results show that the lymphoblastic response to the antigen Pseudomonas aeruginosa of the most affected patient was strongly reduced in comparison to the response of the less affected one. The plasma from the most affected patient contains an inhibitory factor which reduces the lymphoblastic response of the less affected one. On the other hand, plasma from the less affected patient improves the lymphoblastic response of the most affected one (although not significantly). One notes a better lymphoblastic response when the most affected patient's lymphocytes are put in the presence of the less affected one's antigens and plasma. These findings suggest a phenomenon of lymphocyte tolerance in the most affected patient towards P. aeruginosa.

Some immunochemical characteristics of a T-cell-derived ovalbumin (OA) antigen-specific helper (ThF120-OA) and a corresponding OA-specific suppressor effector factor (TsF120-OA) are described. These immunoregulatory molecules are retained by columns containing either the insolubilized antigen OA or the lectin ConA, or antibodies specific for the VH-region of immunoglobulins, for the beta 2-microglobulin or for Ia-framework determinants. Neither the helper factor nor the suppressor factor showed affinity for antisera specific for immunoglobulin isotypes. In search of a constant-region-like structure in factor molecules, antisera were raised in rabbits using ThF120-OA and TsF120-OA. The results show that antisera raised against ThF120-OA recognize one or more determinants of different antigenic specificities common to human ThF. This common structure is not species-specific since it is also recognized by rabbit antisera to mouse helper factor. It is absent, however, on human TsF120-OA. In the same way, human TsF120-OA was shown to interact with rabbit antisera to human (or murine) suppressor factors of different antigenic specificities, but not with anti-ThF.

BALB/c mice were immunized against a monoclonal antiidiotypic antibody (Id 315.1.4) directed against the myeloma DNP-binding protein MOPC315 (IgA-lambda 2). This antibody is specific for an MOPC315 "private" idiotope, and the expression of this idiotope requires the interaction between MOPC315 heavy and lambda chains. Two categories of antibodies, able to combine with Id 315.1.4, were characterized in the sera of anti-Id 315.1.4 mice: (1) antibodies with a kappa light chain and without detectable anti-DNP function, and (2) antibodies with a lambda light chain and able to combine with DNP antigen. This observation suggests that the idiotypic network is not close-ended for a given idiotypic system but must be connected with other systems.

Chromium 51-labelled murine splenocytes were injected intravenously into syngeneic non-immune recipients. The percentages of radioactivity recovered in the spleens and the livers were determined, together with the liver/spleen (L/S) radioactivity ratios. It was found that using trinitrobenzene sulphonate (TNBS)-treated cells resulted in a diminution of splenic recovery, with a concomitant augmentation of the L/S ratio, which corresponded to figures found when non-treated xenogeneic lymphocytes were injected. When using splenocytes modified with trifluoromethyl-dinitrobenzene sulphonate (CF3-DNBS)--an analogue of TNBS--this sort of natural immunity was not observed. As cell modifications with TNBS and CF3-DNBS have previously been shown to cross-react in purely cellular immunity tests, the striking difference observed here was tentatively attributed to differential sensitivity to serum-borne factors which mediate this in vivo natural resistance. These factors are likely to be naturally occurring anti-trinitrophenyl antibodies. Contrastingly, if TNBS- and CF3-DNBS-modified splenocytes were injected into either anti-TNBS or anti-CF3-DNBS immunized mice, the modification of radioactivity recovery and L/S indexes (compared to those in non-immunized controls) was always greater in the case of the CF3-DNBS cells. It is concluded that, of these two cross-reacting cell surface modifying treatments, one (TNBS) is sensitive both to natural and reinforced immunity, whereas the second (CF3-DNBS) is sensitive only to reinforced immunity. As we have previously shown in vitro, that CF3-DNBS-modified cells do not seem to be sensitive to cytotoxic antibodies, we believe that the in vivo immune rejection observed is essentially a cell-mediated reaction, whereas the natural immunity is mainly a serum-dependent reaction.

The method of binding of lipopolysaccharides (LPS) extracted from Salmonella typhimurium to aminohexyl-sepharose 4B by activation with benzoquinone was applied to three different LPS extracted from several enterobacteria species: S. seftenberg 1,3,19, S. cholerae suis 6(2),7 and Escherichia coli O141:H32. It was also used for two polysaccharides (PS) extracted from S. seftenberg 1,3,19 and Streptococcus agalactiae type II strain, respectively. Both PS were free from amino groups but exhibited the corresponding antigenic determinants of the cell wall. The use of these immunosorbents enabled us to obtain a monospecific antiserum. They may be a useful tool for serological identification of salmonella and group B streptococci. This method may be applied for other bacterial surface PS. The possible regeneration of such immunosorbents without appreciable loss of their antigen binding capacity makes possible their use for obtaining monospecific antibodies on a preparative scale.

A new in vitro microassay was devised for the quantitation of macrophage-mediated cytotoxicity on cancer cells. After 72 h of culture with macrophages, the residual adherent target cells were stained with methylene blue. The cell-bound dye was then eluted and measured in a photometer. This assay is simple, quickly performed and gives reproducible results in good correlation with direct counting of the residual cells. It allows a quantitative evaluation of the whole toxic effect (cytostasis and cytolysis) of activated macrophages on adherent tumour cells.

An enzyme-linked immunosorbent assay (ELISA) was developed to monitor the antibody response to Corynebacterium parvum during cancer immunotherapy. Firstly, in sera from 176 clinically healthy individuals not treated with C. parvum, elevated ELISA extinction values were observed from the age of 11 years onwards for both sexes; these high values were probably due to preexisting antibodies to C. parvum or related organisms. Consequently, in order to evaluate C. parvum antibody levels after treatment it was essential to compare post- with pre-treatment sera. Next, a series of sera from 20 male patients with inoperable squamous cell carcinoma of the bronchus were tested. They originated from three different groups. The first group received both chemotherapy (cyclophosphamide) and immunotherapy (C. parvum), the second group cyclophosphamide alone and the third group neither of these agents. Compared to pre-treatment values, an increase in extinction values was already observed as from day 12 of C. parvum treatment; cyclophosphamide did not influence the extinction values. Antibody production per se did not seem to be correlated with an anti-tumour effect. The sensitivity of ELISA was similar to a previously described latex agglutination test.

To gain a better understanding of the antibacterial and antiprotozoal activity of spiramycin as well as the characteristic conditions of cellular defence, we studied its accumulation and intracellular localization in cultured macrophages. Within two hours spiramycin in its active form is accumulated intracellularly by macrophages to a concentration 10 to 20 times that found in the extracellular medium; it is released slowly by the cells when they are incubated in antibiotic-free medium. After differential or isopycnic centrifugation, a bimodal localization of spiramycin was found; one part could be associated with the soluble cytosolic fraction and another with organelles sedimenting at a density of 1.17 g/ml, which represent part of the lysosomal population and perhaps the phagosomes.

The effect of human alpha-1-antichymotrypsin (alpha-1-Achy) on antibody response was studied in mice. alpha-1-Achy increased the number of antisheep erythrocyte antibody-producing cells. The increase was dependent on the dose of alpha-1-Achy injected (from 0.25 to 1 mg par mouse). alpha-1-Achy was effective if injected 2 days before or simultaneously with sheep erythrocytes. Asialylated alpha-1-Achy also enhanced the antibody response in the same way as native alpha-1-Achy. When alpha-1-Achy was heated at 60 degrees C for 15 min, it appeared to maintain immunoenhancing activity. However, when treated at 70 degrees C for 15 min, an intermediate immunoenhancing activity was observed, and heating at 100 degrees C for 15 min resulted in loss of activity.

The production of lymphokines by alloreactive murine T-lymphocyte clones was investigated. Clones derived by limiting dilution or by micromanipulation were stimulated with T-cell-depleted irradiated allogeneic spleen cells, and the resulting supernatants were assayed for interleukin-2 (IL-2), interferon-gamma (gamma-IFN), macrophage-activating factor (MAF), B-cell helper factor (BHF) or granulocyte/macrophage colony-stimulating factor (GM-CSF). Lymphokine production was found to be heterogeneous at the clonal level, with both cytolytic and non-cytolytic clones being able to produce some (or all) of the factors tested. Comparison of a large number of independently derived clonal supernatants allowed the separation of IL-2, BHF and GM-CSF from each other and from MAF and gamma-IFN; however, no dissociation between the latter 2 lymphokines was observed.