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EN
The pathomechanism of Helicobacter pylori action upon gastric mucosa and its role in the pathogenesis of gastritis have not been fully elucidated. The aim of this study was to evaluate the most prevalent lymphocyte subpopulations of the gastric mucosa in gastritis in children, as well as to evaluate the expression of Fas and Fas ligand receptors (FasL), periapoptotic markers of gastric mucosa lymphocytes before and after H. pylori eradication. Forty nine patients aged 6 to 17 years, investigated due to chronic abdominal pain, were studied. The obtained tissue samples were analysed by immunohistochemistry. Different lymphocyte subsets were quantified on the basis of surface antigen expression (CD3, CD4, CD8, CD20), secreted cytokines (IL-4, IL-6, IFNγ) and Fas and FasL proteins in the gastric mucosa. B and T helper lymphocytes were found to play a major role in the inflammatory infiltration in the gastric mucosa in children during H. pylori infection. Their expression was found to decrease after eradication. The enhanced expression of Fas receptor on lymphocytes before treatment and a decrease of this expression after eradication of H. pylori were shown. It was demonstrated that there is a correlation between CD4 and Fas receptor expression that may induce apoptosis of the helper lymphocytes in infected children.
EN
Phosphoantigens (PAgs) activate Vγ9Vδ2 T lymphocytes, inducing their potent and rapid response in vitro and in vivo. However, humans and nonhuman primates that receive repeated injections of PAgs progressively lose their Vγ9Vδ2 T cell response to them. To elucidate the molecular mechanisms of this in vivo desensitization, we analyzed the transcriptome of circulating Vγ9Vδ2 T cells from macaques injected with PAg. We showed that three PAg injections induced the activation of the PPARα pathway in Vγ9Vδ2 T cells. Thus, we analyzed the in vitro response of Vγ9Vδ2 T cells stimulated with a PPARα agonist. We demonstrated that in vitro PPARα pathway activation led to the inhibition of the BrHPP-induced activation and proliferation of human Vγ9Vδ2 T cells. Since the PPARα pathway is involved in the antigen-selective desensitization of human Vγ9Vδ2 T cells, the use of PPARα inhibitors could enhance cancer immunotherapy based on Vγ9Vδ2 T cells.
EN
The laminin receptor precursor (LRP) has been the center of intense controversy and interest for over a decade. Chief among these controversies is the putative multifunctional aspect of this molecule: as a ribosomal-associated protein (p40) and/or as the precursor for the 67kDa high-affinity laminin receptor (67LR), neither of which have been definitively established. Other controversies include the presence of more than one 67kDa laminin receptor protein. However, interest in the molecule is sustained because of its vital function in the cell as a component of the translational machinery and due to its constant up-regulation in cancer cells with the invasive and metastatic phenotype and in association with poor prognosis. Recently, while studying the autoimmunogenicity of a species conserved 37-44 kDa oncofetal antigen (37kDa OFA), the authors of this paper, using amino acid sequencing of isolated OFA-peptides, cDNA cloning and sequencing and antigens-antibodies cross reactivity as well as antigens-T cell recognition reactions, identified the 37kDa OFA as precursor or immature laminin receptor protein.
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