Jorjani Biomedicine Journal

Background & Objectives: Defect in Immune responses, such as immunosuppression is one of the major causes of AML pathogenesis and progression which could be targeted for immunotherapy of these patients. CD200 and IDO are immunoregulatory factors which are overexpressed in some solid tumors and hematological malignancies. Distinct researches have shown that CD200 and IDO expressions are associated with AML progression. In the current study, we simultaneously examined the expression of these molecules, as the two important factors including in immunosuppression, in the newly diagnosed and relapse AML patients to investigate their correlation with each other.

Methods: In this study, 48 Peripheral Blood Mononuclear Cells (PBMCs) samples of newly diagnosed and relapsed AML patients were tested and also 32 PBMCs of normal subjects were employed as normal controls. CD200 expression level was examined on the cells by Flowcytometry and quantitative real time RT-PCR was used to determine the IDO-1 gene expression. Finally data were analyzed statistically by Spss 17 software.

Results: Our data showed that CD200 (P=0.02) and IDO-1 (P=0.44) were overexpressed in AML samples especially in relapsed patients. Comparison between FAB AML subgroups demonstrated no statistical differences regarding CD200 level but expression of IDO-1 was slightly increased only in M4 subgroup in comparison to M3 (P=0.01). Correlation analyses showed strong association between the expressions of CD200 and IDO-1 in all patients particularly in relapsed AML, whereas no significant correlation was found in normal subjects.  

Conclusion: According to the role and overexpression of CD200 and IDO-1 in AML patients and also their two-way correlation with T-reg lymphocytes in disease induction and progression, simultaneous assessment of these parameters are so valuable for more exact prognosis detection. Also inhibition of all these immunoregulatory pathways could be so useful for immunotherapy outcome, especially in relapsed AML.