1Mohamed A Awad, 1Doaa A Aladle, 1Solafa A El-Sharawy and 2Nabil Abd El-Razik
1Hematology Units of Clinical Pathology and 2Pediatric Departments, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Fas ligand (FasL) is a membrane protein that is expressed on
activated T cells and natural killer cells. Soluble FasL (sFasL) binds to Fas
on target cells and induces apoptosis. Interferon- g (IFN- g) is a potent inhibitor of myeloid colony
formation in vitro. In order to investigate the involvement of sFasL and IFN -g in the pathogenesis of bone marrow failure,
we determined serum levels of sFasL and IFN- g in 32 patients of bone marrow failure (12
cases with aplastic anemia, 10 cases with pure red cell aplasia, and 10
patients with chemotherapy-induced hypoplasia) at time of diagnosis and in some
cases after remission. In addition, 13 age-matched healthy controls were
included in the study. sFasL and IFN-g levels were significantly elevated at the
time of diagnosis when compared to those of the control group (p < 0.001). A significant reduction in sFasL and
IFN- g levels was detected after remission in five cases with pure red cell aplasia, who
responded well to immunosuppressive therapy (p < 0.01). A negative
correlation was found between the serum level of both molecules and hemoglobin
concentration, total leukocytic count, absolute neutrophil count, platelet
count, reticulocytic count and bone marrow cellularity. In conclusion, sFasL
and interferon- g
are suspected to play an important role in the pathogenesis of bone marrow
failure and this can be applied to therapeutic interventions.