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Identifying Bone Marrow Microenvironmental Populations in Myelodysplastic Syndrome and Acute Myeloid Leukemia
Published on: November 10, 2023
[Changes of subsets of DC1 in the bone marrow of severe aplastic anemia patients]
Guang-sheng He1, Zong-hong Shao, Hong He
1Institute of Hematology and Blood Disease Hospital, CAMS and PUMC, Tianjin 300020, China.
Insights
Dendritic cell 1 (DC1) subsets, including immature and activated forms, are elevated in severe aplastic anemia (SAA) bone marrow. This imbalance promotes T-cell dysfunction and hematopoietic failure in SAA patients.
Area of Science:
- Immunology
- Hematology
Background:
- Severe aplastic anemia (SAA) is a rare but serious condition characterized by bone marrow failure.
- Dendritic cells (DCs) play a crucial role in immune regulation and T-cell activation.
Purpose of the Study:
- To quantify dendritic cell 1 (DC1) subsets in the bone marrow of SAA patients.
- To investigate the relationship between DC1 subsets and T-cell populations (Th1, CD3+CD8+ cells) and hematopoietic function.
- To explore the role of DC1 in SAA pathogenesis.
Main Methods:
- Flow cytometry (FACS) was used to measure DC1 subsets (CD11c+CD1a+, CD11c+CD83+), Th1 cells, and CD3+CD8+ cells in bone marrow.
- Correlations between these cell populations and hematopoietic parameters (reticulocyte and neutrophil counts) were analyzed.
Main Results:
- SAA patients exhibited significantly higher percentages of Th1 cells, CD11c+CD1a+ cells, and CD11c+CD83+ cells compared to normal controls.
- These percentages decreased significantly in recovering SAA patients.
- Elevated CD3+CD8+ cells in SAA patients negatively correlated with reticulocyte and neutrophil counts.
- CD11c+CD83+ cell percentages positively correlated with Th1 and CD3+CD8+ cells, and negatively with hematopoietic parameters.
Conclusions:
- Both immature and activated DC1 subsets are increased in SAA bone marrow, indicating a shift towards an activated state.
- This DC1 imbalance may drive Th0 cell polarization to Th1 cells, leading to T-lymphocyte over-activation and subsequent hematopoietic failure in SAA.
Objective:
To measure the subsets of dendritic cells 1 (DC1) in the bone marrow of severe aplastic anemia (SAA) patients and evaluate the relationships between the CD11c+CD83+ cells and Th1 cells, CD3+CD8+ cells or hematopoietic function and explore the role of DC1 in the pathogenesis of SAA.
Methods:
By FACS, the quantities and ratios of CD11c+CD1a+ cells, CD11c+CD83+ cells, Th1 cells, and CD3+CD8+ cells in the bone marrow of SAA patients and normal controls were detected respectively. The relationships between CD3+CD8+ cells and reticulocyte absolute value (Ret) or neutrophil absolute value (ANC), between Th1 cells and CD3+CD8+ cells, Ret or ANC, between CD11c+CD83+ cells, and Th1 cells, CD3+CD8+ cells, Ret or ANC were evaluated.
Results:
In normal controls' bone marrow, the percentages of Th1 cells, CD11c+CD1a+ cells, CD11c+CD83+ cells and the ratio of CD11c+CD83+/CD11c+CD1a+ were (0.42 +/- 0.30)%, (0.38 +/- 0.29)%, (0.37 +/- 0.32)% and 1.07 +/- 0.10, respectively. In untreated SAA patients, they were (4.87 +/- 0.54)%, (1.73 +/- 0.24)%, (3.38 +/- 0.56)% and 2.21 +/- 0.32 respectively, which were higher than that in normal controls (P < 0.01). In recovering SAA patients, the percentages of Th1 cells, CD11c+CD1a+ cells and CD11c+CD83+ cells decreased significantly to (0.53 +/- 0.22)%, (0.61 +/- 0.23)%, (0.65 +/- 0.22)%, respectively (P < 0.01). The ratio of CD11c+CD83+/CD11c+ CD1a+ in recovering SAA patients decreased to 1.37 +/- 0.25, which was similar to that in normal controls (P > 0.05). The percentage of CD3+CD8+ cells in untreated SAA patients was (32.32 +/- 10.22)%, and in recovering SAA patients decreased to (13.67 +/- 5.24)% (P < 0.01). The percentage of CD3+CD8+ cells in SAA patients was negatively correlated with their Ret and ANC (P < 0.05), while their Th1 cell percentages were positively correlated with their CD3+CD8+ cells (P < 0.01), and negatively correlated with their Ret and ANC (P < 0.01). SAA patient's CD11c+CD83+ cell percentages were positively correlated with their Th1 cell and CD3+CD8 cells (P < 0.01, P < 0.05), but negatively with their Ret and ANC (P < 0.01).
Conclusion:
Both immature DC1 and activated DC1 increased in the bone marrow of SAA patients, and the balance of DC1 subsets shifted from stable form to active one, which might promote Th0 cells to polarize to Th1 cells, and cause the over-function of T lymphocytes and hematopoiesis failure in SAA.
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