PubMed · 5124405
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1971-11-06. Rosette inhibition test.. https://pubmed.ncbi.nlm.nih.gov/5124405/
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It is known that beta 2 integrins are crucial for leukocyte cell-cell and cell-matrix interactions, and accumulating evidence now suggests that integrins serve not only as a structural link but also as a signal-transducing unit that controls adhesion-induced changes in cell functions. In the present study, we plated human neutrophils on surface-bound anti-beta 2 (CD18) antibodies and found that the small GTP-binding protein p21ras is activated by beta 2 integrins. Pretreatment of the cells with genistein, a tyrosine kinase inhibitor, led to a complete block of p21ras activation, an effect that was not achieved with either U73122, which abolishes the beta 2 integrin-induced Ca2+ signal, or wortmannin, which totally inhibits the phosphatidylinositol 3-kinase activity. Western blot analysis revealed that antibody-induced engagement of beta 2 integrins causes tyrosine phosphorylation of several proteins in the cells. One of these tyrosine-phosphorylated proteins had an apparent molecular mass of 95 kDa and was identified as the protooncogene product Vav, a p21ras guanine nucleotide exchange factor that is specifically expressed in cells of hematopoietic lineage. A role for Vav in the activation of p21ras is supported by the observations that antibody-induced engagement of beta 2 integrins causes an association of Vav with p21ras and that the effect of genistein on p21ras activation coincided with its ability to inhibit both the tyrosine phosphorylation of Vav and the Vav-p21ras association. Taken together, these results indicate that antibody-induced engagement of beta 2 integrins on neutrophils triggers tyrosine phosphorylation of Vav and, possibly through its association, a downstream activation of p21ras.
The migration of human skin fibroblasts into a denuded area in a cell monolayer declined during in vitro and in vivo aging. We carried out a study to determine whether this age-related decline in cell migration was mediated by the autocrine cytokine interferon-beta (IFN-beta), which has been reported to suppress the proliferation, chemotaxis and collagen synthesis of human fibroblasts. Actually, IFN-beta specifically suppressed the migration of TIG-3S human fetal skin fibroblasts into a denuded area in a cell monolayer, as shown by the dose response experiments of IFN-beta and neutralizing anti-IFN-beta antibody. IFN-beta also inhibited their collagen synthesis but the addition of type I collagen could not reverse IFN-beta-induced inhibition of cell migration. Double strand RNA, which has been generally known to induce IFN-beta in human skin fibroblasts, suppressed the migration of TIG-3S cells. Next, a study was done to determine whether IFN-beta and double strand RNA suppressed the migration of TIG-3S cells in late passages as well as early passages, or whether neutralizing anti-IFN-beta antibody stimulated the migration of TIG-3S cells in late and middle passages. IFN-beta and double strand RNA suppressed the migration of TIG-3S cells in middle (PD45) and late (PD55) passages as well as in early passages (PD23-28). Neutralizing anti-IFN-beta antibodies could not reverse the low migratory activity of middle and late passage cells to the high migratory activity of early passage cells. These results indicated that the autocrine cytokine IFN-beta did not seem to be involved in the age-dependent decline of fibroblast migration.
Experimental materno-embryonic transfusions with serum that is immunologically active against blood group antigens cause congenital malformations in the rat embryo. In view of the possible increased incidence of vascular disruptive syndromes after chorionic villus sampling (CVS), we investigated the occurrence of materno-fetal transfusions (MFTs) in this procedure. In 18 pregnant women experiencing two needle introductions at CVS, we looked immunohistochemically at the presence of haemoglobin A1-containing maternal erythrocytes in the fetal circulation of the separately collected first and second chorionic villus samples. In 4 of 18 patients (22 per cent), a significant increase of maternal cells was observed in the second sample compared with the first sample, indicating the occurrence of MFT by CVS. On the rare occasion of maternal immunization against fetal antigens, a CVS-associated MFT might provoke immunological damage to the fetus.