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  • Taken together specific antibodies and SR


    Taken together, specific Sulindac sale and SR-SIM used in the study helped uniquely visualize the distribution of lymphocytes and macrophages with their molecular expression in human cochleae. Using SR-SIM, we verified that resident IBA1-positive macrophages are widely distributed in human cochlea (Liu et al., 2018). Some of these macrophages form contact with CD4+ and CD8+ lymphocytes, especially in the modiolus of human cochleae. Our study is the first revealing T lymphocyte-macrophage interaction using super-resolution immunohistochemistry in freshly fixed, healthy adult human cochleae. The results strengthen the view that, in the human cochlea, antigen presenting cells as well as T lymphocytes form part of the immune network to mediate immune function. Further studies will be performed to identify other immune cells in human cochleae (e.g., T memory cells, T regulatory cells and B cells). Such studies will help more comprehensively understand the immune network in human cochlea and its role in diseases.
    Acknowledgments This study was supported by ALF and private funds from Börje Runögård, Sweden. We are grateful to SciLiyfe Laboratories and the BioVis Platform at the Uppsala University for providing SR-SIM microscope equipment and for personal support throughout the study. This study was partly supported by MED-EL, Inc., Innsbruck, Austria.
    Introduction In the West, chronic lymphocytic leukaemia (CLL) is considered one of the most common leukemias affecting the adult population. However, it is infrequent in the Eastern world. Most of the patients can be asymptomatic at diagnosis whereas others can present with systemic B symptoms, lymphadenopathy, hepatosplenomegaly, and infiltration of bone marrow leading to cytopenias [1]. Up to now, there has been no definite cure for CLL, despite advances in understanding the underlying pathology of the disease [2]. Different mechanisms are used by tumors to cause suppression of the host immune system. Adenosine triphosphate (ATP) hydrolysis by CD39 plays an important role in tumor mediated immune suppression [3]. CD39, which is the main ectoenzyme in the immune system, is expressed Sulindac sale by most B cells, subsets of T cells, and dendritic cells. It aids in inhibiting T-cell and Natural killer (NK) cell responses by hydrolyzing ATP and adenosine diphosphate (ADP) generating adenosine, thus suppressing the immune system. This immunosuppressive pathway protects cancer cells and favors tumor growth [4]. In this study, we hypothesized that elevated levels of the highly immune-suppressive CD39+ T cell population may support and promote the unopposed growth of CLL cells, thereby contributing to a more aggressive clinical course of the disease. We investigated the expression of CD39 on CD4+ T Lymphocytes obtained from patients with CLL by using flow cytometry and (del 6q) by fluorescence in situ hybridization (FISH), its correlation with the disease stage and survival.
    Materials and methods
    Statistical analysis Data entry and data analysis were performed using SPSS software version 20 (Statistical Package for the Social Science, version 20, IBM, and Armonk, New York). Data were presented as number, percentage, mean, standard deviation, standard error, median, and range. The Mann–Whitney U test was used to compare quantitative variables between two groups. A p value < .05 was considered statistically significant. Kaplan–Meier Survival analysis and log rank test were used to detect survival curves.
    Results As shown in Table 1 staging of the cases was performed according to the Standard scoring system (Rai staging). Six patients were at low risk (20%), 13 patients were at intermediate risk (43.3%), and 11 patients were at high risk (36.7%). In our study, CD 39 expression on CD4 T cells in CLL patients was significantly higher compared with the control group (p < .001). According to RAI staging, CD39 expression was significantly higher in high risk group of patients than low and intermediate group with a p value = .04 (Table 2).