Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Objective To investigate the relationship between long-chain intergenic non-coding RNA324 (LINC00324) and immunophenotype in peripheral blood leukocytes of acute myeloid leukemia (AML) patients. Methods Real-time quantitative PCR and bioinformatics databases were utilized to analyze the expression level of LINC00324 in peripheral blood leukocytes and cell lines KG-1, THP-1 and U937 in AML patients. The relationships of the expression level of LINC00324 with the red blood cell and platelet count, the expression levels of LINC00324 and immunophenotypes in 40 AML patients were analyzed by Person correlation analysis. The immunophenotypes included CD14, CD68, CD64, CD11b, CD4, CD45, CD33, HLA-DR, CD163, CD2, CD58, CD117, CD43, CD34, CD99, CD8, CD38, CD10, CD13, CD56, CD7, TdT, CD235a, CD138, CD61, MPO and CD19. Simultaneously, the cBioPortal database datasets (TCGA, NEJM 2013) were used to analyze the clinical characteristics of 173 AML patients, and to analyze the correlations between the expression level of LINC00324 and the peripheral blood blast percentage and white blood cell count in tumor samples. Results The expression of LINC00324 in peripheral blood leukocytes of AML patients was down-regulated, and its expression level was significantly correlated with immunophenotype CD33, red blood cell and platelet count. Analysis of bioinformatics database showed that LINC00324 was under-expressed in myeloid leukemia cell lines. The expression of LINC00324 in AML patients was associated with multiple immunophenotypes such as CD33, CD117, CD11b, CD14 and CD64 and was negatively correlated with peripheral blood blast percentage and white blood cell count. Conclusion LINC00324 may be involved in regulating the differentiation, development and function of immune cells, which providing a new strategy for the development of targeted drugs or treatment of AML.
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PMID:[Correlation analysis between LINC00324 and immunophenotype in peripheral blood leukocytes in patients with acute myeloid leukemia]. 3175 Aug 27

Although substantial progress has been achieved concerning neonatal sepsis, its lethality remains considerably high, and further insights into peculiarities and malfunctions of neonatal immunity are needed. This study aims to contribute to a better understanding of the role of human neonatal granulocyte subpopulations and calgranulin C (S100A12). For this purpose, we gathered 136 human cord blood (CB) samples. CD66b+ CB low-density granulocytes (LDG) and CB normal-density granulocytes were isolated and functionally and phenotypically compared with healthy adult control granulocytes. We could identify CB-LDG as CD66bbright CD64high CD16low CD35low CD10low S100A12med-low and, based on these markers, recovered in whole CB stainings. Consistent with flow cytometric findings, microscopic imaging supported an immature phenotype of CB-LDG with decreased S100A12 expression. In CB serum of healthy neonates, S100A12 was found to be higher in female newborns when compared with males. Additionally, S100A12 levels correlated positively with gestational age independently from sex. We could solidify functional deficits of CB-LDG concerning phagocytosis and generation of neutrophil extracellular traps. Our study reveals that previously described suppressive effects of CB-LDG on CD4+ T cell proliferation are exclusively due to phagocytosis of stimulation beads used in cocultures and absent when using soluble or coated Abs. In conclusion, we characterize CB-LDG as immature neutrophils with functional deficits and decreased expression and storage of S100A12. Concerning their cross-talk with the adaptive immunity, we found no direct inhibitory effect of LDG. Neonatal LDG may thus represent a distinct population that differs from LDG populations found in adults.
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PMID:Cord Blood Low-Density Granulocytes Correspond to an Immature Granulocytic Subset with Low Expression of S100A12. 3244 90


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