Proliferation of bone marrow hematopoietic stem cells and function of T helper lymphocytes of patients with immuno-related pancytopenia.
- Author:
Rong FU
1
;
Zong-hong SHAO
;
Hong LIU
;
Hong HE
;
Juan SUN
;
Ming-feng ZHAO
;
Guang-sheng HE
;
Jun SHI
;
Jie BAI
;
Tian-ying YANG
;
Chong-li YANG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Bone Marrow Cells; cytology; Cell Division; Cells, Cultured; Child; Cytokines; genetics; Female; Hematopoietic Stem Cells; cytology; Humans; Male; Middle Aged; Pancytopenia; immunology; RNA, Messenger; analysis; T-Lymphocytes, Helper-Inducer; physiology
- From: Chinese Journal of Hematology 2004;25(4):213-216
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo explore the proliferative capacity of bone marrow hematopoietic stem cells and the function of T helper (Th) lymphocytes of patients with immuno-related pancytopenia (IRP).
METHODSTwenty-five untreated IRP patients, 15 IRP patients in complete remission (CR) and 10 normal controls were studied for in vitro yields of CFU-GM, CFU-E and BFU-E from bone marrow mononuclear cells (BMMNC). The mRNA expressions of IL-4, IL-10, IFN-gamma and IL-2 genes in unstimulated BMMNC from 25 untreated IRP patients,15 IRP patients in CR, 19 patients with other hematological diseases presenting pancytopenia and 10 normal controls were detected by reverse transcription polymerase chain reaction (RT-PCR).
RESULTSThere was no significant difference of the yields of CFU-E, CFU-GM or BFU-E among the untreated, and in CR IRP patients and normal controls (P > 0.05). The mRNA expressions of IL-4 and IL-10 of Th2 cells were significantly higher in untreated IRP patients than in the other groups. The mRNA expressions of IFN-gamma and IL-2 of the Th1 cells in all IRP patients were not higher than those in the other groups.
CONCLUSIONSThe cytopenia of IRP patients was not caused by the qualitative abnormality of the hematopoietic stem cells but by the destruction or suppression of hematopoietic stem cells from certain extrinsic insults. The imbalance of Th lymphocytes subtypes and overfunction of Th2 lymphocytes played important roles in the pathogenetic mechanism of IRP leading to increased and overfunctional B lymphocytes, which produced autoantibodies destructing or suppressing hematopoiesis in IRP.