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EN
Estrogen (E2) was shown to prevent experimental autoimmune encephalomyelitis (EAE) and to produce a novel population of regulatory CD45dimVLA-4+ cells. Although their appearance was dependent upon an elevated hormonal level, E2 was not required for their production, as they also were induced by immunization with Mycobacterium tuberculosis as a component of complete Freund's adjuvant. Materials and Methods: Molecular techniques, including ribonuclease protection assays and quantitative RT-PCR, were used to provide further characterization of CD45dimVLA-4+ cells. Moreover, we determined the developmental requirements of the CD45dimVLA-4+ cells using genetically modified mice and extensive flow cytometry analysis. Results: Characterization of CD45dimVLA-4+ mRNA profile revealed highly elevated levels of CD16, CD44, CCR3, IP-15, and IL-13 transcripts compared with their CD45highVLA-4+ counterparts. Furthermore, we found up-regulation of anti-apoptotic bcl-w and bcl-xl genes and transcripts encoding the TCR and CD8 homodimer. The production of CD45dimVLA-4+ cells was evident in nude mice and in MHC class II- and 2-microglobulin, but not in CD1-deficient mice, suggesting a crucial role for CD1 in their induction.
EN
Aberrant glycosylation is a common phenomenon accompanying colon carcinoma progression. The changes observed include increased expression of Lewis blood group family antigens, particularly Lex, sialyl Lex and sialyl Lea. Recently it was shown that these antigenic epitopes may play an important role in cell-cell homotypic as well as heterotypic adhesive interactions. This work presents a phenotypic characteristic of 11 human colon carcinoma cell lines of different degree of differentiation expression of potential ligands for endogenous cellular lectins: Lewis antigens, CEA and CD44v6 antigens was evaluated by cytofluorimetry. The aim of the work is to select adhesive and invasive colon carcinoma cells with specified cell surface antigen pattern, for studies on adhesive interactions with endothelial cells, occurring during early steps of metastasis.
EN
It is now well documented that experimental autoimmune encephalomyeltitis (EAE) can be effectively prevented by estrogen therapy. Previously, we identified a limited set of genes that were altered in spleens of mice protected from EAE by 17-estradiol (E2) treatment. As a continuation of these studies, we here present transcriptional changes in genes expressed in spinal cord tissue. The Affymetrix microarray system was used to screen more than 12,000 genes from E2-treated double Tg (BV8S2 and AV4) female mice protected from EAE vs. control mice with severe EAE. We found that estrogen therapy had a profound inhibitory effect on expression of many immune-related genes in spinal cords. Estrogen significantly affected transcription of 315 genes, 302 that were down-regulated and only 13 that were up-regulated by >2.4 fold. A number of genes encoding the histocompatibility complex, cytokines/receptors, chemokines, adhesion molecules, and signal transduction proteins, were strongly down regulated (>20 fold) in estrogen treated mice to levels similar to spinal cord tissue from unmanipulated mice. The identification of genes with altered expression patterns in spinal cords of estrogen treated mice provides unique insight into the process that ultimately results in protection against EAE.
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