Recently, a third evolutionarily conserved gene, NWC, was discovered within the recombination activating gene (RAG) locus, known to contain the RAG1 and RAG2 genes. Here, we identify and characterize the murine endogenous NWC protein which has no homology to any known protein and is ubiquitously expressed. In the cell, the NWC protein which has been suggested to function as a transcriptional repressor, is found in the cytoplasm as well as in the nucleus.
Deoxycytidine kinase (dCK) is one of the key enzymes of deoxynucleoside salvage supplying resting lymphocytes with DNA precursors for synthesis and repair. The level of dCK activity is especially important in chemotherapy with the use of deoxynucleoside analogues like arabinosyl cytosine (Citarabid, ara-C), or 2-chloro-deoxyadenosine (Cladribine, CdA). Previous results showed that Cladribine treatment of human lymphocytes increased several fold the activity of dCK without increasing the amount of dCK protein itself (Sasvári-Székely, et al., 1998, Biochem. Pharmacol. 56, 1175), and a possible post-translational modification was suggested. This theory was further investigated using NaF as an inhibitor of protein phosphatases. It was shown that NaF treatment of cells elevated dCK activity while inhibiting DNA synthesis. The possible mechanism of dCK activation/inactivation induced by exposure of cell cultures to different agents is discussed.
Autoimmune thyroid diseases include several distinct clinical entities, mainly Graves' disease and Hashimoto's thyroiditis. An incompetent immune response directed against the body's own tissues, and the production of antibodies against specific cell antigens accompanied by chronic inflammation, all occur in autoimmune thyroid diseases. The autoimmune process is induced by genetic and environmental factors that are difficult to identify and generates the development of concomitant diseases in other systems. Leukocyte activation and overproduction of inflammatory mediators, as well as improper levels of thyroid hormones, play an essential role in the chronic course of these diseases. The development of autoimmune thyroid diseases results from the impairment of the regulatory and suppressor functions of T-cells or NK cells and activation of B cells, or from the changes in the number of those cells. Many reports have shown the significant role of platelet-leukocyte interaction in inflammation. Autoantibodies react with target antigens in different kinds of cells, including blood platelets, and autoimmune processes can modulate the mutual cooperation of blood platelets and lymphocytes. The activity of blood platelets and lymphocytes is reciprocally regulated. It has been suggested that blood platelets can influence lymphocyte function by direct contact with receptors, and indirectly via soluble mediators. The interactions of platelet-immune cells (neutrophils, monocytes, lymphocyte and dendritic cells) can have a potent enhancing effect on immune cells functions.
The pathogenicity of RHDV (rabbit haemorrhagic disease virus) is mainly associated with its affinity to blood vessels, with causing disseminated intravascular coagulations (DIC), and with the stimulation of the host immune system. Moreover, there are implications suggesting that apoptosis may be a pivotal process in understanding the basis of viral haemorrhagic disease in rabbits - a serious infectious disease causing mortality to wild and domestic rabbits. The aim of this study is to evaluate, by means of flow cytometry, the dynamics of apoptosis in peripheral blood granulocytes and lymphocytes in rabbits experimentally infected with seven different strains of RHDV and so-called antigenic variants of RHDV denominated as RHDVa, i.e.: Hungarian 24V/89, 1447V/96, 72V/2003; Austrian 01-04, 237/04, V-412 and French 05-01. The results showed that all of the RHDV and RHDVa strains cause an increase in the number of apoptotic cells throughout the infection, which might indicate the need for further analysis of the importance of this process.
The present study was undertaken to contribute to the characterization of the degree of variability in baseline damage in white blood cells from control population, and to investigate how this variability is associated with external and internal factors. Altogether 170 healthy volunteers, randomly selected from the general population of the Republic of Croatia, participated in the study. Two sensitive tests: the alkaline comet assay and the chromosome aberration test were applied to study the background levels of DNA damage in their white blood cells. The results point to inter-individual differences, indicating different genome sensitivity. As revealed by both assays, the background levels of DNA damage were mostly influenced by smoking habit as well as medical exposure (especially to diagnostic X-rays). Sex and age of subjects did not significantly influence the values of DNA damage recorded in the white blood cells. Although higher levels of DNA damage were recorded in blood samples collected during winter and autumn, they were mostly influenced by medicinal exposure and smoking habit. Statistical evaluation of the data confirmed that a positive correlation exists between DNA migration and the number of long-tailed nuclei found with the comet assay and the total number of chromosome aberrations. The data obtained can serve as control values in forthcoming biomonitoring studies.
W ostatnich latach nową, dynamicznie rozwijającą się gałęzią nauki o odporności jest immunometabolizm. Dział ten bada jak przemiany metaboliczne zachodzące w komórkach układu odpornościowego, wpływają na ich przetrwanie, rozwój, ale także funkcje wykonawcze. W opracowaniu tym opisujemy przebieg podstawowych i pomocniczych szlaków pozyskania energii przez leukocyty, a w szczególności glikolizę, cykl Krebsa, szlak pentozofosforanowy oraz utlenienie kwasów tłuszczowych. Przedstawiamy znaczenie poszczególnych szlaków dla funkcjonowania leukocytów, rozwoju ich fenotypu (np. makrofagów M1 i M2), oraz przełączania szlaków podczas ich aktywacji. Zmiany te mogą wpływać na funkcje obronne w czasie reakcji zapalnej, infekcji lub uszkodzenia tkanek. Z drugiej strony, leukocyty mogą realizować różne programy metaboliczne, celem pozyskania energii do walki z patogenami. Zależność pomiędzy funkcjami obronnymi a metabolizmem rzuca także nowe światło na zrozumienie mechanizmów chorób metabolicznych, a przede wszystkim kompleksowej odpowiedzi immunologicznej.
EN
In recent years, a new branch of immunology called immunometabolism has been established. The discipline focuses on intracellular metabolic changes in immune cells that impact - influence their survival, development, as well as defense mechanisms. Here we provide a brief summary of basic and ancillary metabolic pathways which leukocytes utilize to obtain energy, with a special focus on glycolysis, TCA cycle, penthosophosphate pathway and fatty acid oxidation. Significance of the given metabolic path for leukocyte functioning, phenotype changes (e.g. M1 vs. M2 macrophages) and biochemical changes during activation is discussed. The metabolic changes can in fact shape the effector functions during inflammation, infection or tissue injury. On the other hand, leukocytes can adopt different metabolic programs to gain energy required to eliminate pathogens. An interplay between immunity and metabolism sheds new light on understanding of metabolic diseases but foremost on complex immune responses.
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