No abstract

Histamine has been reported to exert an inhibitory effect on the growth of transplanted tumors(5). The present results are in accord with this observation.Since tumor growth was more favorable in histamine depleted animals, it is tempting to assume that tissue reactivity or inflammatory potential regulates tumorigenesis. In order to determine to what extent this hypothesis could further be verified, experiments are now underway to investigate whether compound 48/80 might influence the rate of tumor induction in rats.Summary. The growth of Walker Tumor 256 is increased in rats receiving compound 48/80 in progressive dosage. This is significant only in animals pretreated with the histamine releaser.

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Data on microgeographic population structure on four neighbouring villages of Sardinia island (Italy) are presented and discussed. Two villages are located in the lowlands where malaria from Plasmodium falciparum was endemic until the eradication of paludism. The other two villages are located in the highlands and they were malaria-free because of the altitude. Census data, inbreeding, migration matrices and surname distributions have been collected. The genetic differentiation of the four villages, tested for 31 genetic polymorphisms (106 alleles), is only in part compatible with migration rates inferred from demographic data. The possible adaptive nature of some genetic markers with respect to malarial resistance is discussed. Ambiguous results from population genetics quantitative methods do not support definite answers.

T cells recognize protein antigens as fragments (peptides) held in a defined binding site of class I or class II major histocompatibility (MHC) molecules. The formation of complexes between various immunologically active peptides and different MHC molecules has been demonstrated directly in binding studies between the peptides and solubilized, purified molecules of class II MHC. Studies with intact cells, living or fixed, have not directly demonstrated the binding of the peptides to MHC molecules on antigen-presenting cells, but the formation of such complexes has been shown indirectly through the capacity of antigen-presenting cells to stimulate specific T cells. Here we report evidence that supports directly the binding of radiolabelled influenza matrix peptide 17-29 to products of the human class II MHC locus HLA-DR, on living homozygous B-cell lines, and we show that the kinetics of such binding is much faster with living cells than with fixed cells. Furthermore, whereas the peptide reacts with HLA-DR molecules of all alleles, it binds preferentially to DR1, the restricting element in antigen presentation.