Abstract
Objective We studied bone marrow plasma (BMP) cytokines in severe aplastic anemia (SAA) patients and healthy volunteers to investigate differences in the cytokine profiles between them and propose a cytokine signature of SAA. Methods A Bio-Plex suspension array system was used to measure 27 analytes in BMP samples from 47 SAA patients and 30 healthy donors. Results Compared to healthy people, SAA patients had higher levels of tumor necrosis factor α (TNF-α (TNF-γ (IFN-γ (IFN-β (MIP-1β (MIP-1α (TNF-α (TNF-β (MIP-1β (MIP-1β (MIP-1γ (IFN-α (TNF-Conclusions The current study demonstrated distinct cytokine profiles among untreated SAA patients, recovering SAA (RSAA) patients, and healthy people. The cytokines of RSAA patients showed similar characteristics to those of untreated SAA patients and healthy people, respectively, which may reflect that the immune status of RSAA patients is in different stages of recovery after IST; thus, it may provide an important tool in diagnosing and evaluating or predicting curative effects in clinics.
Highlights
Severe aplastic anemia (SAA) is a severe disease characterized by bone marrow failure and a high fatality rate
In the present study, increased levels of Type I lymphocyte factors IFN-c, IL-2, and tumor necrosis factor α (TNF-α) were observed in the bone marrow plasma (BMP) of untreated SAA patients; these levels decreased after immunosuppressive therapy (IST)
Ese results are consistent with the theory of SAA immune pathogenesis, which suggests that SAA is an autoimmune disease that results from overactivation of the immune system, especially T lymphocytes [1, 2]
Summary
Severe aplastic anemia (SAA) is a severe disease characterized by bone marrow failure and a high fatality rate. Bone marrow failure in SAA is usually caused by an immunologic mechanism, and immunosuppressive therapy (IST) is effective in most SAA patients [1, 2]. Cytokines and chemokines play a key role in immune cell activation in the pathogenesis of SAA. Cytokines and chemokines are lowmolecular-weight proteins that are secreted by immunocytes, activate other immune cells, and mediate inflammatory responses. IFN-c, TNF-α, and IL-2 levels have been shown to significantly increase in SAA [4, 5]. The immune pathogenesis of SAA has been widely studied, very little is known about the alternations of cytokines and chemokines in the bone marrow
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