Browsing by Subject "immunophenotyping"

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    Immunophenotyping in acute myeloblastic leukemia: Review; [Akut miyeloblastik lösemide i̇mmünofenotipik deǧerlendirme]
    (2010) Gülen H.
    Acute myeloid leukemia is a heterogeneous disease, presenting with a high diversity of phenotypes. Immunophenotyping is essential for diagnosis and definition of particular myeloid leukemia subtypes such as M0, M7 and M3 variants which cannot be defined by cytomorphology or cytochemistry alone. M0 blasts show minimally antigenic differentiation and also morphologically resemble to FAB L1/L2 blasts of lymphoblastic leukemia. Additionally, it can express TdT and lymphoid associated antigens such as CD2, CD4, CD7, CD10, CD19 and can be diagnosed falsely as myeloid antigen positive lymphoblastic leukemia. cyCD3, CD5 and cyCD79a antigens are the best markers in differantation of M0 and lymphoblastic leukemia. HLA-DR and CD34 are the best markers in differantation of M3 and other subtypes of myeloid leukemia. In this sense, CD14 is also a valuable marker, because it is not reported in any case of promyelocytic leukemia. M7 subtypes of myeloid leukemia can not be diagnosed by routine cytochemical dyes unless immunophenotyping. The establishing of CD41 (gpIIb) and/or CD61( gpIIIa)positivity and myeloperoxidase negativity on blasts by immunophenotyping can confirm megakaryoblastic leukemia diagnosis. Recently, immunophenotyping of blast cells by flow cytometry plays an increasing role in diagnosis and following of minimal residual disease. The antigens assosciated with poor prognosis in myeloid leukemia are CD7, CD56 and CD34. A phenotype of CD117+CD34+CD15+ is expressed in many myeloid leukemia subgroups and is used in following of minimally residual disease during remission. In conclusion, CD13, CD33, HLA-DR, CD34, CD117, CD11, CD14, CD15, CD41, CD61, MPO, CD65, cyCD3, CD7, cyCD79a, and CD19 markers should be studied in all cases of myeloid leukemia at presentation. Copyright © 2010 by Türkiye Klinikleri.
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    The investigation of immunomodulatory effects of adipose tissue mesenchymal stem cell educated macrophages on the CD4 T cells
    (Elsevier GmbH, 2019) Özdemir R.B.Ö.; Özdemir A.T.; Sarıboyacı A.E.; Uysal O.; Tuğlu M.İ.; Kırmaz C.
    Mesenchymal stem cells (MSCs) are strong immunomodulatory cells investigated in numerous clinical studies on fatal pathologies, such as graft versus host disease and autoimmune diseases; e.g., systemic lupus erythematosus, Crohn's disease, and ulcerative colitis. Macrophages are one of the critical cells linking the innate and adaptive immune system, and it has been shown that MSCs can differentiate between pro-inflammatory M1 phenotype and anti-inflammatory M2 phenotype of macrophages. However, it has not yet been fully clarified whether these differentiated macrophages are functional. In this study, we compared the immunomodulatory effects on the CD4 T cells of M1, M2a and M2c macrophages with the macrophages that directly and indirectly cultured with MSCs. We analyzed the changes in CD14, CD64, CD80, CD163 and CD200R expression to evaluate macrophage phenotypes, and the changes in CD4, IFN-g, IL-4, IL-17a and FoxP3 expression to evaluate T helper subsets using the FACS method. The changes in IL-1b, IL-4, IL-10, IL-12p70, IL-17a and IFN-g in the media supernatants were analyzed using the Luminex method. We also performed WST-1 and Caspase-3 ELISA analyses to observe the proliferation and apoptosis status of the T cells. MSCs were found to differentiate macrophages into a distinctive phenotype, which was close to the M2c phenotype, but was not considered as an M2c cell due to the low expression of CD163, a characteristic marker for M2c. While MEM-D, MEM-ID and MSCs showed similar inhibitory effects on the Th2 and Th17 cells, the most significant increase in Treg cell frequencies was seen in MEM-D cells. Macrophages can alter their phenotypes and functions according to the stimuli from the environment. The fact that macrophages educated with MSCs suppressed the production of all the cytokines we evaluated even after the removal of MSCs suggests that these cells may be differentiated by MSCs into a suppressive macrophage subgroup. However, the Treg cell activation caused by direct interactions between MSCs and macrophage cells may be the most prominent observation of this study compared to previous work. As a result, according to our data, the interactions between MSCs and macrophages may lead to differentiation of macrophage cells into an immunosuppressive phenotype, and these macrophages may suppress the T lymphocyte subgroups at least as effectively as MSCs. However, our data obtained from in vitro experiments should be supported by future in vivo studies. © 2019 Elsevier GmbH
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    Successful management of delayed-onset adenosine deaminase deficiency with novel mutation
    (Newlands Press Ltd, 2024) Çelik F.Ç.; Soyöz Ö.; Bölük S.Ö.; Taşklrdl I.; Hacl I.A.; Kaya M.A.; Demir A.; Uzunoǧlu B.; Ylldlrlm A.T.; Onay H.; Gözmen S.; Gülez N.; Genel F.
    A 4-year-old boy presented with acute-onset autoimmune cytopenia with severe, persistent lymphopenia, autoimmune thyroiditis, elevated IgE and glucose 6-phosphate dehydrogenase enzyme deficiency. In immunologic evaluation, lower T, B and natural killer cells and higher levels of adenosine deaminase (ADA) metabolites were observed. The compound heterozygous novel ADA gene mutations causing ADA deficiency were detected. Successful immunologic and metabolic cure was achieved with enzyme replacement therapy, followed by reduced intensity conditioning hematopoietic stem cell transplantation from a matched unrelated donor. An interesting aspect of this patient is the detection of novel compound heterozygous mutations without consanguinity and a secondary outcome is the recovery of glucose 6-phosphate dehydrogenase deficiency after hematopoietic stem cell transplantation. © 2023 Future Medicine Ltd.