Toxic shock syndrome toxin 1 (TSST-1) is a potent immunomodulating substance isolated from Staphylococcus aureus strains associated with toxic shock syndrome (TSS). Flow cytometric analysis was used to compare scatter changes in several cell-surface phenotype markers on human mononuclear cells exposed in vitro to TSST-1 or to phytohemagglutinin, a lectin with similar effects on the immune response. The results showed differences between PHA and TSST-1 in the appearance of the tested T cell subset markers and of interleukin 2 receptors. In general, the stimulation of mononuclear cells by TSST-1 was slower than that by phytohemagglutinin. TSST-1 induced the production of interferon in cultures of murine spleen cells. By means of inhibition studies with specific antibodies to interferon, the interferon produced was characterized as the gamma type. Human mononuclear cells exposed to the toxin also produced gamma interferon, with levels similar to those induced by staphylococcal enterotoxin A, a known potent interferon inducer. The induction of gamma interferon by TSST-1 may play a role in the immunosuppression caused by TSST-1.

Adult↗

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Susceptibility to murine hepatitis virus (type 3)-induced paralysis is influenced by class I genes of the MHC.

Using H-2 recombinant congenic strains of mice, genetic analysis of resistance to murine hepatitis virus type 3 (MHV3)-induced paralysis was performed. It appeared that both H-2K and H-2D, two class I gene regions of the mouse major histocompatibility complex (MHC), can play independent significant roles in the establishment of such resistance.

Animals↗

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Oral administration of killed Brucella abortus may increase immunity.

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Adjuvants, Immunologic↗

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[Hybrid effects].

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Animals↗

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Natural and reinforced immunity against hapten-modified cells in vivo: importance of serum-borne and cellular factors.

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.

Animals↗

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[Relationship between tumor antigens and histocompatibility antigens at the cell membrane].

The authors outline schematically the major histocompatibility complex as well as the relationship between tumor neo-antigen and pre-existing antigens at the cell surface. They note that these two antigenic systems are not independent and in particular, the major histocompatibility system (H-2) co-segregates with the tumour antigens. Considering the complexity of the H=2 system (a H-2 allele does not correspond to any single transplantation antigen but to a combination of several antigens units simultaneously present), the authors recall Boyse's hypothesis, revised by Haywood and Mc Khann, which propose that tumour antigens are a rearrangement of H-2 substructures. Moreover, it is possible that the relationship between H-2 and resistance to cancer may be attributed directly to the action of genes controlling the immune response (Ir region) which could also intervene in recognition of these tumour antigens. Finally, recent results obtained seem to show that some tumour antigens cross-react with H-2 fractions. This fact prevents the mice bearing these types of alleles from being immunized against the cross-reacting tumours. If this result could be transposed to the human situation, it would explain the frequency of certain types of tumours in defined H-LA groups and could allow the prediction of high-risk groups.

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