Journal
ANNALS OF HEMATOLOGY
Volume 84, Issue 9, Pages 572-577Publisher
SPRINGER
DOI: 10.1007/s00277-005-1022-8
Keywords
aplastic anemia (AA); interferon-gamma (IFN-gamma); tumor necrosis factor-alpha (TNF-alpha); hematopoiesis; apoptosis
Categories
Ask authors/readers for more resources
Immune-mediated stem cell damage has been postulated to be responsible for disease initiation and progression in aplastic anemia (AA). It is hypothesized that T lymphocytes play a major role in destroying the bone marrow (BM) stem cells of AA patients by infiltrating the BM and secreting excessive levels of anti-hematopoietic cytokines, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha). We undertook this study to assess the pathogenic significance of anti-hematopoietic cytokines such as IFN-gamma and TNF-alpha in BM T cells and plasma of AA patients. Significantly elevated levels of IFN-gamma and TNF-alpha were found in the BM plasma of AA patients compared to controls (p=0.05 and 0.006, respectively). Intracellular IFN-gamma and not TNF-alpha in BM CD3(+) T cells of AA patients was significantly higher compared to controls (p=0.04 and p=0.2, respectively). A follow-up analysis of expression of these cytokines in BM T cells and their levels in BM plasma in five AA patients before and 180 days (6 months) after antithymocyte globulin (ATG) and cyclosporin A (CsA) therapy showed a decline 180 days after therapy compared to pre-therapy. We thus conclude that increased production of both IFN-gamma and TNF-alpha in the BM may contribute to disease pathogenesis in AA and ATG therapy may induce hematological remission by suppressing the elevated levels of IFN-gamma and TNF-alpha in AA BM.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available