K. Hamzaoui, A. Hamzaoui, H. Houman
Homeostasis and Cell Dysfunction Unit Research, La rabta Hospital, Behçet`s disease unit reseach,Tunis, Tunisia
2006 Vol.24, N°5 ,Suppl.42 - PI 0071, PF 0078
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To investigate whether the CD4<sup>+</sup>CD25<sup>+</sup> regulatory T cell (Treg) population, which plays important role in autoimmune diseases is related to the pathophysiology of Behçet`s disease (BD).
Forty-two patients with BD (20 patients in active disease) fulfilling the criteria of the International Study Group of BD. Twenty age-matched healthy controls were studied. We analyzed CD4<sup>+</sup>CD25<sup>+/high</sup> T cells and the mRNA expression of Foxp3, cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), and transforming growth factor Β (TGF-Β) in BD. We have studied the ability of CD4<sup>+</sup>CD25<sup>+</sup> (Treg) to regulate proliferation of CD4<sup>+</sup>CD25<sup>-</sup> T cells during active BD stage.
Active BD patients had significantly higher CD4<sup>+</sup>CD25<sup>+/high</sup> T cells, as compared with BD in the remission stage, and healthy controls. There was no significant differences in the CD4+ CD25<sup>+/high</sup> T cells expression between healthy controls and remission BD. In active BD, mRNA for Forkhead box p3 (Foxp3) and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) were highly expressed when compared to remission BD and healthy controls. There was no differences in the mRNA expression for TGF-Β in active BD, remission BD and healthy controls. Functionally, CD4+CD25<sup>+/high</sup> T cells in active BD were impaired in their proliferative responses and could suppress the proliferation of their CD4<sup>+</sup>CD25<sup>-</sup> counterparts.
These data demonstrate that CD4<sup>+</sup>CD25<sup>+</sup> Treg cells, with the potential to regulate suppression of effector T cells, were increased in the peripheral circulation of active BD patients. The role of CD4<sup>+</sup>CD25<sup>+/high</sup> T cells in the regulatory process of the inflammation in active BD, could be taken in account.
PMID: 17067431 [PubMed]