Cell-mediated lysis of autologous platelets in chronic idiopathic thrombocytopenic purpura

:  Objectives: Investigate the contribution and mechanism of cell‐mediated cytotoxicity to the pathogenesis of idiopathic thrombocytopenic purpura (ITP). Methods: We observed the cytotoxic effect of cytotoxic T‐lymphocyte (CTL) (CD8+) and natural killer cells (CD3−CD16+CD56+) toward chronic ITP pati...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:European journal of haematology 2006-05, Vol.76 (5), p.427-431
Hauptverfasser: Zhang, Feng, Chu, Xiaoxia, Wang, Lin, Zhu, Yuanyuan, Li, Lizhen, Ma, Daoxin, Peng, Jun, Hou, Ming
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung::  Objectives: Investigate the contribution and mechanism of cell‐mediated cytotoxicity to the pathogenesis of idiopathic thrombocytopenic purpura (ITP). Methods: We observed the cytotoxic effect of cytotoxic T‐lymphocyte (CTL) (CD8+) and natural killer cells (CD3−CD16+CD56+) toward chronic ITP patient's autologous platelets, and investigated the expression of Fas ligand (FasL), tumor necrosis factor (TNF)‐α and TNF‐related apoptosis inducing ligand, as well as perforin and granzyme B mRNA in CD8+ cells using flow cytometry and reverse transcriptase‐polymerase chain reaction. Results: We found that platelet lysis was seen only using purified CD8+ T cells as effector cells; expression of FasL and TNF‐α in CD8+ T cells in ITP group was elevated. Moreover, the mRNA levels of granzyme B and perforin in CD8+ cells of ITP patients were increased. Conclusions: Our findings suggest that CTLs are activated in chronic ITP and might be involved in the pathogenesis of this disorder. Apoptosis and perforin/granzyme‐mediated cytotoxicity constitute an important pathway through which CTLs destruct autologous platelets. CTLs might be a reasonable target for a therapeutic strategy.
ISSN:0902-4441
1600-0609
DOI:10.1111/j.1600-0609.2005.00622.x