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Phenotypic Profiles (phenotypic + profile)
Selected AbstractsPhenotypic profile and functional characterization of rat lymph node-derived ,, T cells: implication in the immune response to cytomegalovirusIMMUNOLOGY, Issue 2 2003Larissa Dyugovskaya Summary ,, T cells are unique, and their localization at sites of infection is considered critical in immune defence. We demonstrate the accumulation of ,, T cells in rat regional popliteal lymph nodes (PLNi) starting 2 days after inoculation of cytomegalovirus (CMV) into the footpad. Early-appearance PLNi ,, T cells significantly inhibited plaque development and the spread of CMV infection. These ,, T cells were negative for CD4 and CD8beta receptors, proliferated in response to interleukin-2 (IL-2) and contained high levels of interferon-, (IFN-,), the appearance of which correlated with the curing of fibroblasts from virus infection. The addition of anti-IFN-, abolished the ability of fibroblast monolayers to be cured from CMV infection. In contrast, this protection was not abolished by the addition of anti-rat IL-2 or anti-rat TNF-,, or by the depletion of NKR-P1-bearing cells within ,, T cells. In addition, the present study shows that while ,, T cells derived from naive and CMV-infected rats are able to kill both YAC-1 targets and CMV-infected syngeneic fibroblasts in vitro, only the latter are able to clear CMV-infected fibroblast monolayers. Finally, our data suggest that the expression of NKR-P1 by ,, T cells is critical for cytotoxicity, but its contribution to the curing from CMV infection was limited. [source] Exceptional good cognitive and phenotypic profile in a male carrying a mosaic mutation in the FMR1 geneCLINICAL GENETICS, Issue 2 2007LCP Govaerts Fragile X (FRAX) syndrome is a commonly inherited form of mental retardation resulting from the lack of expression of the fragile X mental retardation protein (FMRP). It is caused by a stretch of CGG repeats within the fragile X gene, which can be unstable in length as it is transmitted from generation to generation. Once the repeat exceeds a threshold length, the FMR1 gene is methylated and no protein is produced resulting in the fragile X phenotype. The consequences of FMRP absence in the mechanisms underlying mental retardation are unknown. We have identified a male patient in a classical FRAX family without the characteristic FRAX phenotype. His intelligence quotient (IQ) is borderline normal despite the presence of a mosaic pattern of a pre-mutation (25%), full mutation (60%) and a deletion (15%) in the FMR1 gene. The cognitive performance was determined at the age of 28 by the Raven test and his IQ was 81. However, FMRP expression studies in both hair roots and lymphocytes, determined at the same time as the IQ test, were within the affected male range. The percentage of conditioned responses after delay eyeblink conditioning was much higher than the average percentage measured in FRAX studies. Moreover, this patient showed no correlation between FMRP expression and phenotype and no correlation between DNA diagnostics and phenotype. [source] Immunophenotypic analysis of the Kaposi sarcoma herpesvirus (KSHV; HHV-8)-infected B cells in HIV+ multicentric Castleman disease (MCD)HISTOPATHOLOGY, Issue 5 2008A Chadburn Aims:, Kaposi sarcoma herpesvirus (KSHV) is aetiologically related to Kaposi sarcoma, classical and extracavitary primary effusion lymphoma (PEL; EC-PEL) and multicentric Castleman disease (MCD), entities preferentially occurring in HIV-infected individuals. Characterization of HIV-associated PELs/EC-PELs suggests that the KSHV-infected malignant cells originate from a pre-terminal stage of B-cell differentiation. However, only limited phenotypic studies have been performed on HIV+ MCD, including for PR domain containing 1 with zinc finger domain/B lymphocyte-induced maturation protein 1 (PRDM1/BLIMP1), a key regulator of terminal B-cell differentiation. The aim was to characterize KSHV-infected cells in 17 cases of HIV+ MCD. Methods and results:, Double immunohistochemistry and immunohistochemistry,in situ hybridization were used to characterize the KSHV-infected cells in MCD; the results were compared with the phenotypic profiles of 39 PELs/EC-PELs and seven PEL cell lines. Whereas the immunophenotype of KSHV-infected cells in MCD and malignant KSHV+ PEL cells was similar (PAX5, Bcl-6,; PRDM1/BLIMP1, IRF4/MUM1+; Ki67+), the MCD KSHV-infected cells differed, as they expressed OCT2, cytoplasmic , immunoglobulin; variably expressed CD27; lacked CD138; and were Epstein,Barr virus negative. Conclusions:, Although both PEL and MCD originate from KSHV-infected pre-terminally differentiated B cells, these findings, with previously reported genetic studies, indicate HIV+ MCD may arise from extrafollicular B cells, whereas PELs may originate from cells that have traversed the germinal centre. [source] Differentiation of Streptococcus mutans and Streptococcus sobrinus via genotypic and phenotypic profiles from three different populationsMOLECULAR ORAL MICROBIOLOGY, Issue 1 2001Y. Li Routine identification of Streptococcus mutans and Streptococcus sobrinus is generally based upon growth on various selective media, colony morphology and biochemical characteristics. We examined various approaches of differentiating these two species through a combination of the conventional phenotypic methodology with chromosomal DNA fingerprint (CDF) and arbitrarily primed polymerase chain reaction (AP-PCR) methods. Initially, ten ATCC type strains and 20 randomly selected clinical isolates of mutans streptococci (MS) were characterized and grouped into two major types based on patterns generated by the CDF using HaeIII digestion. The CDF's patterns with restriction fragments equal to or greater than 6.6 kb were defined as the CDF-1 group. The CDF's patterns with restriction fragments less than 6.6 kb were defined as the CDF-2 group. Both groups were then examined for biotype, serotype, and composition of DNA via thermal denaturation. AP-PCR was applied and evaluated for the capability of delineating S. mutans from S. sobrinus strains. Results of this study showed that all CDF-1 strains fit within a G+C range of 36.2% to 42.2%, whereas the CDF-2 strains had a G+C range of 45.8% to 47.0%. The serotyping assay exhibited 100% sensitivity, 90% specificity and 86.7% agreement with the CDF. The biotyping assay presented the poorest specificity (38.5%), indicating the highest variability. The capability of AP-PCR in differentiation of S. mutans from S. sobrinus was comparable to the CDF method, suggesting that either of these two approaches can and may serve as a viable alternative method to serotyping or biotyping of MS. [source] Circulating endothelial microparticles as a marker of cerebrovascular disease,ANNALS OF NEUROLOGY, Issue 2 2009Keun-Hwa Jung MD Objective Circulating endothelial microparticles (EMPs) have been reported to reflect vascular damage. Detailed profiling of these blood endothelial markers may adumbrate the pathogenesis of stroke or enable determination of the risk for stroke. We investigated EMP profiles in patients at risk for cerebrovascular disease. Methods We prospectively examined 348 consecutive patients: 73 patients with acute stroke and 275 patients with vascular risk factors but no stroke events. We quantified various types of EMPs by flow cytometry using CD31, CD42b, annexin V (AV), and CD62E antibodies in the peripheral blood of patients. This method allowed fractionation of CD31+/CD42b,, CD31+/AV+, and CD62E+ EMPs. Clinical and laboratory factors associated with EMPs were assessed. Results Recent ischemic episodes were found to be more strongly associated with greater CD62E+ EMP levels than with levels of other phenotypes. Increased National Institutes of Health Stroke Scale scores and infarct volumes in acute stroke patients were significantly associated with greater CD62E+ EMP levels. In the risk factor group, patients with extracranial arterial stenosis had greater CD62E+ EMP levels, whereas those with intracranial arterial stenosis had greater CD31+/CD42b, and CD31+/AV+ EMP levels. The ratio of CD62E+ to CD31+/CD42b, or CD31+/AV+ EMP level significantly discriminated extracranial and intracranial arterial stenosis. Interpretation Circulating EMP phenotypic profiles reflect distinct phenotypes of cerebrovascular disease and are markers of vascular pathology and an increased risk for ischemic stroke. Ann Neurol 2009;66:191,199 [source] |