Published online before print September 7, 2006
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* Laboratoire dImmunogénétique-Allergologie, Centre de Recherche Public de la Santé (CRP-Santé), Luxembourg-City, Luxembourg; and
Service de Médecine Interne, Clinique Médicale B, Hôpitaux Universitaires de Strasbourg, Strasbourg, France
1Correspondence: Laboratoire dImmunogénétique-Allergologie, Centre de Recherche Public de la Santé (CRP-Santé), 84 Val Fleuri, L-1526 Luxembourg, Luxembourg. E-mail: jacques.zimmer{at}crp-sante.lu
Regulatory T cells (Treg) are key players in the maintenance of peripheral tolerance. As a result of suppressive effects on CD4+ and CD8+ effector T cells, Treg control the adaptive immune system and prevent autoimmunity. In addition, they inhibit B lymphocytes, dendritic cells, and monocytes/macrophages. It is interesting that several recent papers show that CD4+CD25+ Treg are also able to inhibit NK cells. Thus, Treg exert their control on immune responses from the onset (triggering of innate immune cells) to the effector phase of adaptive immunity (B and T cell-mediated responses). That Treg inhibit NK cells suggests that their uncontrolled activation might break self-tolerance and induce "innate" autoimmune pathology. Conversely, Treg-mediated suppression of NK cell functions might have negative effects, as these cells are important in defense against infections and cancer. It is conceivable that Treg might dampen efficient activation of NK cells in these diseases.
Key Words: suppression inhibition TGF-ß NKG2D
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