The association between AA and GSTT1 deletion suggests a role of glutathione-conjugation in AA, possibly through protecting the hematopoietic compartment from endogenous metabolites or environmental exposures.
Several case-control studies linked homozygous deletion of the glutathione S-transferase theta (GSTT1) gene to AA; however, the role of GSTT1 deletion remains controversial as other studies failed to confirm the association.
Genetic polymorphism of the detoxifying enzymes, the glutathione-S-transferase (GST) and microsomal epoxide hydrolase (mEh), with alteration in their activities could explain the genetic interindividual risks for AA.
We analyzed the impact of the polymorphisms in CYP4501A1 and GSTM1 and GSTT1 genes on the susceptibility and disease severity in 200 patients with AA and compared the frequency with the normal population.
The aim of the study was to characterize the genetic polymorphism of biotransforming phase I (p450-cyp2E1) and phase II [microsomal epoxide hydrolase (mEh), glutathione S-transferase (GST)] enzymes in pediatric patients with acquired aplastic anemia.
The GSTT1 null genotype (absence of both alleles) was associated with a significantly increased risk for acquired aplastic anemia (odds ratio, 2.8; 95% confidence interval, 0.15-5.7).
We have investigated the expression of RNA transcripts of hematopoiesis regulatory molecules, viz., macrophage inflammatory protein (MIP)-1<i>α</i>, tumor necrosis factor (TNF)-<i>α</i>, granulocyte colony-stimulating factor (G-CSF), stromal cell-derived factor (SDF)-1<i>α</i>, stem cell factor (SCF), and transforming growth factor (TGF)-<i>β</i> in lipopolysaccharide-induced bone marrow mesenchymal stem cells (BM-MSCs) and levels of their soluble forms in the culture supernatants of BM-MSCs and BM plasma of patients with acquired aplastic anemia (AA) (<i>n</i> = 29) and controls (<i>n</i> = 29).
The markedly high prevalence of leukocytes lacking HLA-B4002 as a result of either 6pLOH or structural gene mutations, or both, suggests that antigen presentation by hematopoietic stem/progenitor cells to cytotoxic T cells via the HLA-B allele plays a critical role in the pathogenesis of AA.
Recently enhanced T-helper type 17 (Th17) immune responses and deficient CD4(+) CD25(hi) FoxP3(+) regulatory T cells (Tregs) have been reported in acquired aplastic anemia (AA).
Recently enhanced T-helper type 17 (Th17) immune responses and deficient CD4(+) CD25(hi) FoxP3(+) regulatory T cells (Tregs) have been reported in acquired aplastic anemia (AA).
CD4(+)CD25(+) regulatory T cells (Tregs) were believed to control development and progression of autoimmunity by suppressing autoreactive effector T cells, but little was known regarding the function of Tregs in AA.
CD4(+)CD25(+) regulatory T cells (Tregs) were believed to control development and progression of autoimmunity by suppressing autoreactive effector T cells, but little was known regarding the function of Tregs in AA.
We report on a female patient with acquired aplastic anemia whose bone marrow cells showed DNA rearrangement of the immunoglobulin-JH region that disappeared after 1 month with recovery of hematopoiesis through treatment with granulocyte colony-stimulating factor (G-CSF) and immunosuppressive drugs.
Interleukin-2 (alias: IL-2, TCGF, Lymphokine), a type of interleukin, is also a potent signalling molecule in the signalling cascade of the immune-mediated activation of T Lymphocytes leading to the destruction of haematopoietic stem cell (HSC) which is the basis of acquired aplastic anaemia (AAA).
We have investigated the expression of RNA transcripts of hematopoiesis regulatory molecules, viz., macrophage inflammatory protein (MIP)-1<i>α</i>, tumor necrosis factor (TNF)-<i>α</i>, granulocyte colony-stimulating factor (G-CSF), stromal cell-derived factor (SDF)-1<i>α</i>, stem cell factor (SCF), and transforming growth factor (TGF)-<i>β</i> in lipopolysaccharide-induced bone marrow mesenchymal stem cells (BM-MSCs) and levels of their soluble forms in the culture supernatants of BM-MSCs and BM plasma of patients with acquired aplastic anemia (AA) (<i>n</i> = 29) and controls (<i>n</i> = 29).