Decreased Percentage (decreased + percentage)

Distribution by Scientific Domains


Selected Abstracts


Influence of HLA-DR2 on perforin-positive cells in pulmonary tuberculosis

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 5 2007
D. N. Rajeswari
Summary Perforin is one of the key effector molecules of cytotoxic T cells and natural killer cells. The influence of HLA-DRB1 alleles on peripheral blood perforin-positive CD4, CD8, CD16 and CD56 cells was studied by flow cytometry. HLA-DRB1 typing was done in normal healthy subjects (NHS: n = 156) and patients with pulmonary tuberculosis (PTB: n = 102) by polymerase chain reaction-based sequence-specific oligonucleotide hybridization method. We observed a significantly decreased percentage of total perforin-positive cells (per+) (P = 0.0004); CD8+/Per+ (P = 0.0005); CD16+/Per+ (P = 0.05) and CD56+/Per+ cells (P = 0.001) in HLA-DR2-positive PTB patients compared to non-DR2 patients. Subtyping of HLA-DR2-positive subjects at the allelic level revealed that the percentage of CD8+/Per+ cells did not differ among DRB1*1501 and DRB1*1502 patients while a trend towards a decreased percentage of CD16+/Per+ and CD56+/Per+ cells was noticed in DRB1*1501 patients compared to DRB1*1502 patients. The present study suggests that HLA-DR2 may be associated with down-regulation of perforin-positive cytotoxic lymphocytes and natural killer cells in pulmonary tuberculosis. [source]


Immunodeficiency with recurrent panlymphocytopenia, impaired maturation of B lymphocytes, impaired interaction of T and B lymphocytes, and impaired integrity of epithelial tissue: A variant of idiopathic CD4+ T lymphocytopenia?

PEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2002
Horst Von Bernuth
Idiopathic CD4+ T lymphocytopenia (ICL) has been defined as a cause of immunodeficiency with a variable clinical course and an unknown etiology. Here we describe a now 18-year-old boy with ICL, chronic mucocutaneous candidiasis (CMC), recurrent abscesses, and relapsing aphthous and ulcerous lesions. In addition to ICL the patient frequently showed a panlymphocytopenia. An increased percentage of ,+,+ T lymphocytes and IgD+ IgM+ B lymphocytes, and a decreased percentage of CD21+ B lymphocytes, were observed. In vitro assays showed normal T-cell responses to candidin and T-cell mitogens, but impaired B-cell responses to pokeweed mitogen (PWM). B-cell maturation after stimulation with Staphylococcus aureus Cowan I (SAC) and interleukin 2 (IL-2) was nearly normal. The clinical course of the patient improved substantially on administration of constant low-dose therapy with fluconazole. [source]


ORIGINAL ARTICLE: Tumor Necrosis Factor-,-Associated Mechanisms Affecting the Embryonic Response to Cyclophosphamide

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2009
Keren Mammon
Problem, We have previously shown that TNF-,,/, embryos are more sensitive to the exposure to cyclophosphamide (CP) compared with TNF-,+/+ embryos; however, the underlying mechanisms are not fully understood. Thus, in our present study, we tried to identify those molecules that might be responsible for the protective effect of the cytokine. Method of study, CP-treated TNF-,,/, and TNF-,+/+ embryos were analyzed for changes in apoptosis by TUNEL and flow cytometry, while cell proliferation was analyzed by BrdU incorporation. The expression of Bax, bcl-2, p53, the p65 subunit of NF-,B and I,B, was assessed by Western blotting and immunohistochemistry. Results, CP-treated TNF-,,/, embryos exhibited a more profound decrease in their weight, which was accompanied by an earlier appearance of cellular damage and apoptotic cells and an earlier decrease in cell proliferation in the embryonic brain compared with TNF-,+/+ embryos. Also, an increased percentage of Bax-positive cells and a decreased percentage of bcl-2-positive cells were detected in TNF-,,/, embryos 48 hr after exposure, which were accompanied by a decreased percentage of p53-positive cells. Conclusion, Our data implicate TNF-, to be involved in the protection of the embryo against CP teratogenicity, possibly via alteration in Bax, bcl-2 or p53 expression. [source]


Impairment of endothelial cell differentiation from bone marrow,derived mesenchymal stem cells: New insight into the pathogenesis of systemic sclerosis

ARTHRITIS & RHEUMATISM, Issue 6 2007
P. Cipriani
Objective Systemic sclerosis (SSc) is a disorder characterized by vascular damage and fibrosis of the skin and internal organs. Despite marked tissue hypoxia, there is no evidence of compensatory angiogenesis. The ability of mesenchymal stem cells (MSCs) to differentiate into endothelial cells was recently demonstrated. The aim of this study was to determine whether impaired differentiation of MSCs into endothelial cells in SSc might contribute to disease pathogenesis by decreasing endothelial repair. Methods MSCs obtained from 7 SSc patients and 15 healthy controls were characterized. The number of colony-forming unit,fibroblastoid colonies was determined. After culture in endothelial-specific medium, the endothelial-like MSC (EL-MSC) phenotype was assessed according to the surface expression of vascular endothelial growth factor receptors (VEGFRs). Senescence, chemoinvasion, and capillary morphogenesis studies were also performed. Results MSCs from SSc patients displayed the same phenotype and clonogenic activity as those from controls. In SSc MSCs, a decreased percentage of VEGFR-2+, CXCR4+, VEGFR-2+/CXCR4+ cells and early senescence was detected. After culturing, SSc EL-MSCs showed increased expression of VEGFR-1, VEGFR-2, and CXCR4, did not express CD31 or annexin V, and showed significantly decreased migration after specific stimuli. Moreover, the addition of VEGF and stromal cell,derived factor 1 to cultured SSc EL-MSCs increased their angiogenic potential less than that in controls. Conclusion Our data strongly suggest that endothelial repair may be affected in SSc. The possibility that endothelial progenitor cells could be used to increase vessel growth in chronic ischemic tissues may open up new avenues in the treatment of vascular damage caused by SSc. [source]


Decreased expression of germinal center,associated nuclear protein is involved in chromosomal instability in malignant gliomas

CANCER SCIENCE, Issue 11 2009
Kazutaka Ohta
Malignant glioma (MG) is highly proliferative and invasive, with the malignant characteristics associated with aneuploidy and chromosomal instability (CIN). Here, we found that the level of germinal center,associated nuclear protein (GANP), a mammalian homologue of yeast Sac3, was markedly decreased in MGs with a poor prognosis; and thus we explored the effect of its decrease on cell-cycle progression of MG cell lines. Glioblastomas showed a significantly lower level of ganp mRNA than anaplastic astrocytomas, as measured by real-time reverse transcription-PCR, in 101 cases of adult MG. MGs of ganpLow expression displayed more malignant characteristics, with loss of heterozygosity on chromosome 10, epidermal growth factor receptor gene amplification, and significantly poorer prognosis than the ganpHigh group. Human diploid fibroblasts depleted of ganp mRNA by the RNA interference (RNAi) method showed a decreased percentage of S-phase cells and a cellular-senescence phenotype. MG cell lines harboring abnormalities of various cell-cycle checkpoint molecules displayed slippage of mitotic checkpoints and an increased proportion of hyperploid cells after ganp RNAi-treatment. These results suggest that GANP protects cells from cellular senescence caused by DNA damage and that a significant decrease in GANP expression leads to malignancy by generating hyperploidy and CIN. (Cancer Sci 2009); 00: 000,000) [source]


CD3 expression distinguishes two ,,T cell receptor subsets with different phenotype and effector function in tuberculous pleurisy

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009
N. Yokobori
Summary Tuberculous pleurisy is a naturally occurring site of Mycobacterium tuberculosis (Mtb) infection. Herein, we describe the expression of activation, natural killer (NK) and cell migration markers, as well as effector functions from ,,T cells in peripheral blood (PB) and pleural effusion (PE) from tuberculosis patients (TB). We observed a decreased percentage of circulating ,,T from TB patients and differential expression of NK as well as of chemokine receptors on PB and PE. Two subsets of ,,T cells were differentiated by the CD3/,,T cell receptor (,,TCR) complex. The ,,TCRlow subset had a higher CD3 to TCR ratio and was enriched in V,2+ cells, whereas most V,1+ cells belonged to the ,,TCRhigh subset. In PB from TB, most ,,TCRhigh were CD45RA+CCR7 - and ,,TCRlow were CD45RA+/,CCR7+CXCR3+. In the pleural space the proportion of CD45RA - CCR7+CXCR3+ cells was higher. Neither spontaneous nor Mtb -induced interferon (IFN)-, production was observed in PB-,,T cells from TB; however, PE-,,T cells showed a strong response. Both PB- and PE-,, T cells expressed surface CD107a upon stimulation with Mtb. Notably, PE-,,TCRlow cells were the most potent effector cells. Thus, ,,T cells from PB would acquire a further activated phenotype within the site of Mtb infection and exert full effector functions. As ,,T cells produce IFN-, within the pleural space, they would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a T helper type 1 profile. [source]