Natural CD4/CD25 super(+) regulatory T cells control the burst of superantigen-induced cytokine production: the role of IL-10

• Published in: International immunology Vol. 14; no. 2; pp. 233 - 239
• Main Authors: Pontoux, C, Banz, A, Papiernik, M
• Format: Journal Article
• Language: English
• Published: 01-02-2002
• Subjects: CD25 antigen; CD4 antigen
• ISSN: 0953-8178

In normal mice a subpopulation of CD4 T cells constitutively expresses the IL-2 receptor alpha chain (CD25). This natural CD4/CD25 super(+) subset is thymus-born, constitutively expresses IL-10 mRNA, does not produce IL-2 and is resistant to apoptosis. These cells behave as regulatory T cells in the control of self-tolerance, inflammatory reactions and T cell homeostasis. The mechanisms by which natural CD4/CD25 super(+) cells control the immune response is unclear. We examined CD25-deficient mice, which over-express various cytokines, including proinflammatory molecules, after bacterial superantigen stimulation in vivo. We observed that this abnormal cytokine production could be controlled by the injection of natural CD4/CD25 super(+) T cells and that IL-10 production is needed, as CD4/CD25 super(+) T cells from IL-10 knockout mice do not correct cytokine over-production in vivo. As the circulating IL-10 produced by CD25-deficient mice was ineffective, we deduced that the key source of IL-10 was the regulatory T cell population. IL-10 is also involved in the control of cytokine production by normal T cells. However, the target of IL-10 in this control is undefined. Whether it acts directly on the effector T cells or on the regulatory CD4/CD25 super(+) T cells themselves to induce their functional maturation has to be clarified.