Article citationsMore>>
Mokhtar, G.M., El-Beblawy, N.M., Adly, A.A., Elbarbary, N.S., Kamal, T.M. and Hasan, E.M. (2016) Cytokine Gene Polymorphism [Tumor Necrosis Factor-Alpha (−308), IL-10 (−1082), IL-6 (−174), IL-17F, 1RaVNTR] in Pediatric Patients with Primary Immune Thrombocytopenia and Response to Different Treatment Modalities. Blood Coagulation & Fibrinolysis, 27, 313-323.
https://doi.org/10.1097/MBC.0000000000000431
has been cited by the following article:
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TITLE:
Expression and Significance of Regulatory B Cells in Patients with Immune Thrombocytopenia
AUTHORS:
Wei Qian, Xiaoxia Zhang
KEYWORDS:
Immune Thrombocytopenia, CD19+ CD24hiCD38hi Breg, Cytokines
JOURNAL NAME:
Open Journal of Blood Diseases,
Vol.12 No.2,
June
30,
2022
ABSTRACT: Objective: To
detect the expression and significance of regulatory B cells in patients with
immune thrombocytopenia. Methods: 73 ITP patients were divided into
glucocorticoids treatment group (n = 42) and recombinant human thrombopoietin
(rhTPO) treatment group (n = 31). According to the therapeutic effect, it was
divided into effective group and ineffective group. The expression of CD19+
CD24hiCD38hi Breg in peripheral blood was detected by flow cytometry before and
after treatment. The expression levels of transforming growth factor (TGF)-β1, interleukin (IL-10) and interferon
(IFN)-γ were detected by ELISA before
and after treatment. 30 volunteers were selected as the control group. Results: The expression of CD19+ CD24hiCD38hi Breg and cytokines IL-10
and TGF-β1 in 73 ITP patients before
treatment was lower than that in the control group, while the expression of
IFN-γ was higher than that in the
control group (p β1 in the effective
group were significantly higher than before treatment, while the expression of
IFN-γ was significantly lower than before treatment (p + CD24hiCD38hi Breg, IFN-γ,
IL-10 and TGF-β1 in the invalid group
had no significant change compared with before treatment. Conclusion: Abnormal expression of CD19+ CD24hiCD38hi Breg and related cytokines is
involved in the pathogenesis of ITP.