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Immune Cell Populations (immune + cell_population)
Selected AbstractsORIGINAL ARTICLE: Antigen-presenting Cells in Pregnant and Non-pregnant Human MyometriumAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Marina Ivanisevic Citation Ivanisevic M, Segerer S, Rieger L, Kapp M, Dietl J, Kämmerer U, Frambach T. Antigen-presenting cells in pregnant and non-pregnant human myometrium. Am J Reprod Immunol 2010; 64: 188,196 Problem, Inflammatory cells play a crucial role in human parturition. Different populations of leucocytes invade the reproductive tract. Numerous studies have described the decidual immune cell population in pregnant and non-pregnant endometrium. However, little is known about the presence of immune cells in human myometrium. Method of study, We herein analysed a spectrum of immune cells in human myometrium comparing tissue samples from non-pregnant (n = 8) and pregnant (n = 10) uteri. Applying immunohistochemistry with a panel of antibodies specific for T cells, monocytes, natural killer cells, B cells and antigen-presenting cells (CD4, CD8, CD14, CD15, CD16, CD19, CD56, CD68, CD83, HLA-DR, DC-Sign, mast cell tryptase), we characterized the immune cell population of human myometrium. Results, A significantly higher number of CD14, CD15, CD16, DC-SIGN as well as CD4-positive cells were found in myometrium of pregnant compared to non-pregnant uteri, while mast cells were significantly reduced in pregnant myometrium. Conclusion, All markers found increased in pregnant myometrium indicate monocyte/macrophage lineage cells and thus suggest a possible involvement of these cells in healthy pregnancy maintenance. Monocytes/macrophages might produce a microenvironment that permits a controlled invasion of trophoblast cells into the myometrium while preventing a rejection of the semiallogenic conceptus and providing an important barrier against invading pathogenes. [source] DNA vaccines against chronic lung infections by Pseudomonas aeruginosaFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2-3 2003J Staczek Abstract Vaccines containing outer membrane protein F (OprF) of Pseudomonas aeruginosa are effective in reducing lesion severity in a mouse pulmonary chronic infection model. One OprF-based vaccine, called F/I, contains carboxy oprF sequences fused to oprI in an expression vector. When delivered three times biolistically by gene gun, the F/I vaccine induces protection that is antibody-mediated in outbred mice. To demonstrate the role of F/I -induced antibody-mediated immunity, B-cell-deficient [B(,)] and B-cell-intact [B(+)] mice were immunized with F/I, challenged with Pseudomonas, and examined for lesion severity. As expected, F/I -immunized B(+) mice had fewer and less severe lesions than vector-immunized B(+) mice. However, surprisingly, F/I - and vector-immunized B(,) mice were equally protected to levels similar to F/I -immunized B(+) mice. Examination of immune cell populations and cytokine levels indicated a relative increase in the quantity of CD3+ T-lymphocytes in vector- or F/I -immunized and challenged B(,) mice compared to B(+) mice. These data indicate the protective role played by cell-mediated immunity in B(,) mice, which supports our hypothesis that cell-mediated immunity can play an important role in protection against P. aeruginosa. [source] TNF-, from monocyte of patients with pre-eclampsia-induced apoptosis in human trophoblast cell lineJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2007Hiroyuki Seki Abstract Objective:, In pre-eclampsia, fetal growth restriction is frequently observed, and the possible involvement of inhibitory substances on trophoblast cell proliferation and differentiation has been suggested. The objective of this study was to investigate the effects humoral factors, such as cytokines, produced in immune cells on proliferation of an immortalized trophoblastic cell line (TCL) that we established. Methods:, Serum and lymphocyte layers were isolated from the blood of normal pregnant and preeclamptic women. The lymphocyte layer was further fractionated into different immune cell populations by the Stem Sep method. Immortalized trophoblastic cells were cultured with the sera diluted. The cytokine concentrations in the supernatants of lymphocyte cultures were compared between normal pregnancy and pre-eclampsia. The number, DNA content and induced apoptosis were examined on the immortalized trophoblastic cells at the end of culture. Results:, The sera from preeclamptic women significantly inhibited the immortalized trophoblastic cell proliferation in comparison with those from normal pregnancy. Among the lymphocyte fractions, monocytes significantly inhibited the immortalized trophoblastic cell proliferation. The monocytes from preeclamptic women were found to produce higher levels of tumor necrosis factor-, (TNF-,) in the culture supernatant than those from normal pregnant women. The coculture with the monocytes from preeclamptic women increased the frequency of TUNEL-positive TCL cells. TNF-, inhibited immortalized trophoblastic cell proliferation in a dose-dependent manner and induced apoptosis. Conclusion:, The present results suggest that monocytes are activated and that cytokines, such as TNF-,, which is produced by monocytes, induce apoptosis and inhibit proliferation of trophoblast cells in pre-eclampsia. [source] Autoimmunity, spontaneous tumourigenesis, and IL-15 insufficiency in mice with a targeted disruption of the tumour suppressor gene Fus1,THE JOURNAL OF PATHOLOGY, Issue 5 2007AV Ivanova Abstract The Fus1 gene resides in the critical 3p21.3 human chromosomal region deleted in lung and breast cancers. Recently, the tumour suppressor properties of Fus1 were confirmed experimentally by intra-tumoural administration of Fus1 that suppressed experimental lung metastasis in mice. We generated Fus1 -deficient mice that were viable, fertile, and demonstrated a complex immunological phenotype. Animals with a disrupted Fus1 gene developed signs of autoimmune disease, such as vasculitis, glomerulonephritis, anaemia, circulating autoantibodies, and showed an increased frequency of spontaneous vascular tumours. Preliminary analysis of immune cell populations revealed a consistent defect in NK cell maturation in Fus1 null mice that correlated with changes in the expression of IL-15. Injection of IL-15 into Fus1 knockout mice completely rescued the NK cell maturation defect. Based on these results, we propose the hypothesis that Fus1 deficiency affects NK cell maturation through the reduction of IL-15 production but does not directly alter their developmental capacity. Since acquired immunity was not affected in Fus1 -deficient animals, we suggest a relationship between the Fus1 protein and the regulation of innate immunity via IL-15 production. The increased frequency of spontaneous cancers and the development of an autoimmune syndrome in Fus1 null mice imply that these mice could serve as a model for studying molecular mechanisms of anti-tumour immunity and autoimmunity. Published in 2007 by John Wiley & Sons, Ltd. [source] | ||||||||||