ORIGINAL ARTICLE |
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Year : 2014 | Volume
: 39
| Issue : 3 | Page : 122-127 |
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The usefulness of immunoglobulin-like transcript-3 receptor expression in the diagnosis of acute myeloid leukemia with monocytic differentiation
Maha Atfy MD 1, Hoda F Ebian1, Ashraf M Elhefni2, Hebatallah H Atteia3
1 Department of Clinical Pathology, Hospitals of Zagazig University, Zagazig University, Zagazig, Egypt 2 Department of Hematology and Medical Oncology, Faculty of Medicine, Zagazig University, Zagazig, Egypt 3 Department of Biochemistry, Faculty of Pharmacy, Zagazig University, Zagazig, Egypt
Correspondence Address:
Maha Atfy Department of Clinical Pathology, Hospitals of Zagazig University, Faculty of Medicine, Zagazig University, Zagazig 44519 Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1110-1067.148235
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Background Immunoglobulin like transcript (ILT3) is an immunohibitory transmembrane receptor expressed by plasmacytoid dendritic cells (PDCs), monocytoid dendritic cells (MDCs), and monocytes/macrophages. ILT3 has been previously utilized as a highly sensitive and specific marker for the identification of aggressive chronic lymphocytic leukemia (CLL) and to distinguish AML with monocytic differentiation from other types of AML.
Aim and Methods0 Therefore, in the current study, we investigated the diagnostic impact of ILT3 receptor expression in 72 Egyptian patients having AML with monocytic differentiation and 20 healthy volunteer using flow cytometry technique.
Results Our results demonstrated significant overexpression of ILT3 receptor (P < 0.001) in all AML cases displaying monocytic differentiation patients. ILT3 receptor expression was positively correlated with CD4, CD14, CD64, CD11c, MPO and NSE.
Conclusion These data present a significant role for ILT3 receptor expression in combination with CD14, CD64, MPO and NSE in diagnosis of AML with monocytic differentiation. Further clinical studies should be directed towards ILT3 receptor blockade as a future target for AML immunotherapy. |
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