Introduction. The B7 family of molecules: B7.1 (CD80), B7.2 (CD86) and the CD28 receptor are important molecular structures involved in the formation of specific immune responses. Analysis of the features of their expression level in relation to the course of acute myeloid leukemia (AML) is of great interest.

The aim of the work was to evaluate the intensity of expression of costimulatory molecules of the B7 family (B7.1/CD80, B7.2/CD86) on a clone of tumor cells and monocytes; of the CD28 receptor on CD3 – T-lymphocytes in patients with AML before the start of treatment and after specific therapy.

Materials and  methods. Immunological studies were conducted in 17 patients (12 women and 5 men) with AML in the first acute period before and after specific treatment. The co-expression of co-stimulatory molecules of the B7 family (B7.1/CD80, B7.2/CD86) by tumor cells with CD34+, CD117+, CD33+ and CD28 ligand CD3+ T-lymphocytes was analyzed using a ductal laser cytofluorimetry method on a FACScan cytofluorimeter (Becton Dickinson, USA) ). The Statsoft Statistica 6.0 program package was used for statistical data processing. The estimation of the probability of discrepancies was carried out using the non-parametric Mann-Whitney U-test. Differences were considered significant at p<0.05.

Results. It was shown that in AML patients, before the start of treatment, a clone of PC tumor cells with an immunophenotypic profile of CD34+-, CD117+-, CD33+– has, on average, a different level of intensity of expression of costimulatory molecules of the B7 family (B7.1/CD80, B7.2/CD86) and CD28 receptor. Thus, in 1 group (n=7) of patients, more CD34+-, CD117+-, CD33+-, tumor cells with a high intensity of expression of costimulatory molecules of the B7 family (CD80+bright CD86+bright) were found. Whereas in patients of group 2 (n=10), the content of CD34+-, CD33+-, CD117+– tumor cells with a low level of intensity of expression of costimulatory molecules CD80 low, CD86+ low is higher in the blood. In patients in group 1, the number of CD3+bright lymphocytes with a high intensity of expression of the CD28 ligand was on average significantly (p<0.05) higher, and CD3+low was lower than similar indicators in group 2 (p<0.05). In patients with GML before therapy (n=10), the number of CD3+CD28+bright cells in the blood was significantly reduced (p<0.05), and CD3+CD28 low compared to patients after therapy (n=6) with tumor cells in CM and PC. The number of PC CD3+CD28+ low cells in both groups has no significant differences. In patients with AML in remission (n=7), a higher average number of CD33+ monocytes with a high level of intensity of expression of CD80+bright CD86+bright molecules was found in PC. Whereas in patients after therapy with tumor cells in CM, on average, significantly more monocytes with a low level of intensity of expression of costimulatory molecules CD80+low CD86+low compared to patients in remission. According to research data, remission was not achieved in 10 patients with AML after therapy. Among them, in 4 patients, tumor cells were found in the CM, and in 6 – in the CM and PC. In the PC of these patients before therapy, tumor cells mainly expressed a low level of costimulatory molecules CD80+low CD86+low and the ligand CD28 low on T-lymphocytes. The results of immunological studies showed that after therapy with tumor cells in the CM and PC, there remains on average a significant number of cells with a low level of expression of CD80+low CD86+low molecules and a reduced number of CD80+bright, CD86+bright compared to patients of group 1 before therapy. But when compared with patients of group 2 before therapy, no significant differences in the average number of cells with a low level of expression of the CD80+low molecule are observed. At the same time, the content of cells with a high level of expression of the CD86+bright molecule was reduced in patients after PC therapy. It was found that in patients with AML in remission (n=7), the content of CD3+CD28+bright cells in PC was on average increased (p<0.05), and CD3+CD28+ low was significantly reduced (p<0.05) relative to the data in patients after therapy (n=4) who had tumor cells in their CM. The evaluation of the results shows that in AML patients there was a relationship between the low level of intensity of expression of molecules of the B7 family (B7.1/CD80, B7.2/CD86) and CD28 ligand by T-lymphocytes with the course of the disease. Thus, the violation of antitumor immune defense in AML patients depends on the low level of intensity of expression of costimulatory molecules CD80+-, CD86+– on a clone of tumor cells with immunophenotypic features of CD34+-, CD117+-, CD33+– and CD28+ ligand on CD3+ lymphocytes.

Conclusions. The violation of antitumor immune defense in patients with AML depends on the low level of intensity of expression of costimulatory molecules CD80+-, CD86+– on a clone of tumor cells with immunophenotypic features of CD34+-, CD117+-, CD33+– and CD28+ ligand on CD3+lymphocytes.

Keywords: acute myeloid leukemia, costimulatory molecules, tumor cells, monocytes, ligand.