Abstract
To evaluate the balance between T-cell immunoglobulin and mucin domain (Tim) molecules(Tim)-1 and Tim-3 in patients with aplastic anemia (AA), plasma IFN-γ and IL-4 levels were measured in patients with active AA (n = 41), AA in remission (n = 29) and in healthy subjects (n = 40) by enzyme linked immunosorbent assay (ELISA). Using real-time quantitative polymerase chain reaction (RT-PCR), the mRNA expression of IFN-γ, IL-4, Tim-1 and Tim-3 were studied in all subjects. The results showed that the expression of Tim-3 in newly diagnosed patients was significantly deceased, compared with the controls. Meanwhile, Tim-1 mRNA expression in the active AA group was not significantly reduced, which resulted in a declined ratio of Tim-3/Tim-1 in patients with active disease. During the remission stages, the levels of these transcription factors were comparable with those observed in the healthy controls. These findings are the first data on the expression of the Tim-1 and Tim-3 molecules in AA. The reduced levels of Tim-3/Tim-1 in PBMCs during the active stages of disease suggest that they may play a possible role in the pathogenesis and course of AA.
Highlights
Acquired aplastic anemia (AA) is mostly considered as an immune-mediated bone marrow failure syndrome, which differs from the other conditions associated with inherited mechanisms [1]
There was no correlation between the IFN-γ or IL-4 levels and white blood cell, hemoglobin, and platelet counts in the individuals examined in our present study
Aplastic anemia (AA) is a rare, potentially life-threatening failure of hematopoiesis that is characterized by pancytopenia and bone marrow aplasia
Summary
Acquired aplastic anemia (AA) is mostly considered as an immune-mediated bone marrow failure syndrome, which differs from the other conditions associated with inherited mechanisms [1]. A variety of immune molecules, including interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and interleukins (ILs), which are produced by DCs, T lymphocytes and Recent investigations into the mechanisms that regulate the activation and function of CD4+ T cells have shown that T cell immunoglobulin-mucin (Tim) proteins are important regulators of immune function. Studies in mice have indicated that Tim-1 is involved in T helper cell differentiation and suggested that the protein is a positive regulator of T cell activity [9,10]. The gene encoding the Tim-1 protein has been considered as an important atopy susceptibility gene and is associated with Th2 T cell responses [11], suggesting that Tim-1 controls critical regulatory pathways in the immune system
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