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Published on: March 26, 2018
T-lymphocyte sub-populations in orbito-ocular granulocytic sarcoma (OOGS) and acute myelocytic leukemia (AML): a
A O Cavdar1, E Babacan, S Gözdasoglu
1Pediatric Hematology and Oncology Research Center, School of Medicine, Ankara University, Turkey.
Insights
Children with Oral-Genital Syndrome (OOGS) and acute myeloid leukemia (AML) exhibit reduced T cell counts, suggesting a potential cellular immune deficiency underlying their condition.
Area of Science:
- Immunology
- Hematology
- Pediatrics
Background:
- The etiology of Generalized Somatization (GS) and Oral-Genital Syndrome (OOGS) is unclear, with limited knowledge regarding immune function in affected patients.
- Previous observations indicated that children with OOGS, often from lower socioeconomic backgrounds, displayed diminished delayed hypersensitivity and reduced T cell counts.
Purpose of the Study:
- To evaluate T cell subpopulations (CD3, CD4, CD8, CD16) and immunoglobulin levels (IgA, IgM, IgG) in patients with OOGS and AML before treatment.
- To investigate potential links between immune system status and OOGS/AML.
Main Methods:
- Flow cytometry using monoclonal antibodies (CD3, CD4, CD8, CD16) to determine T cell subpopulations.
- Quantitative immunoglobulin level determination (IgA, IgM, IgG).
- Comparison of immune cell counts and immunoglobulin levels between 10 OOGS/AML patients and control groups.
Main Results:
- Significantly lower percentages of Pan T (CD3), CD4, and CD8 cells were observed in OOGS/AML patients compared to controls (p < 0.01).
- Slightly elevated immunoglobulin levels suggested preserved B cell function.
- These findings indicate a cellular immune deficiency in the studied patient group.
Conclusions:
- Preliminary data suggest that cellular immune deficiency may be an underlying factor in OOGS and AML.
- Further research is warranted to elucidate the role of immune competence in these conditions.
Abstract:
The aetiology of GS remains obscure and a little is known about the immune competence of these patients. Interestingly, all children with OOGS were from low 'socio-economic status' and showed diminished delayed hypersensitivity reactions and reduced T cell counts (E-R) in our previous observation. We present herewith a preliminary data on evaluation of T cell sub-populations determined by monoclonal antibodies (CD3, CD4, CD8 and CD16 cells) in 10 patients with OOGS and AML prior to treatment. Quantitative immunoglobulin determinations of IgA, IgM, IgG were also made. The percentage of Pan T (CD3), CD4, CD8 cells were significantly lower than those in the controls (p < 0.01). The immunoglobulin levels were slightly elevated suggesting normal B cell functions. In conclusion, these preliminary findings suggest that cellular immune deficiency may be an underlying cause.

