Assessment of soluble natural killer group 2d ligand (MHC Class I A and UL16 Binding Protein 1) in Iraqi patients with acute myeloid leukemia.

Autor: Mtashar, Baan, Ashoor, Zainab, Shabeeb, Zeyad, Matti, Bassam
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Zdroj: Mustansiriya Medical Journal (MMJ); Jul-Dec2022, Vol. 21 Issue 2, p171-177, 7p
Abstrakt: Background: Acute myeloid leukemia (AML) is "a heterogeneous disease," defined by a wide range of genetic alterations and molecular mutations that have an effect on clinical outcomes and could be used to develop new drugs. In AML, the immune system is tricked and actively suppressed by leukemia itself and by mechanisms that leukemia picked up through further mutations under suppression of selection. Myeloblasts in Acute myeloid leukemia can evasion the naturak killer cell killing by many ways , one of the these way ,the myelocblast cells shed NKG2D soluble ligand (MIC A/B and or ULPB 1-6) in blood and bound to NKG2D activation receptor which lead to inhibit activation of NK cells. The Aim of Study: The aim of this study assessment of Soluble ligand (MICA and ULPB-1) in patients with AML. Patients and Methods: Thirty patients newly diagnosed as AML were enrolled in this study, 24 patients out of 30 were follow up after 14 days of tratment. after 30 days of treatment we get result of therapy. twenty healthy looking persons were considered as control subjects. We used ELISA technique to detection the level of soluble legand (MICA and ULPB-1). Results: The study showed that in order level of sMICA, there were significant differences in AML patients at diagnosis and after 14 days of treatment in comparison to control subjects while there were no significant differences in the level of sULPB1 between AML patients at diagnosis and after 14 days of treatment in comparison to control subjects. Conclusion: This study showed that there was an elevated level of sMICA in AML patients at diagnosis and 14 days to treatment while there was no elevated level of sULPB1 in comparison to the control group. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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