Fc-gamma RIII: The Alternative To The TCR For NKT Cell-activation

A small subpopulation of T cells known as NKT cells (because in addition to proteins expressed by other T cell-populations they also express markers of NK cells, which are a distinct immune cell-type) promotes disease in an antibody-induced mouse model of arthritis. But researchers have yet to determine how the NKT cells are activated to cause disease in this model of arthritis. In a study appearing online on August 17 in advance of print publication in the September issue of the Journal of Clinical Investigation, Doo Hyun Chung and colleagues from Seoul National University College of Medicine show that engagement of Fc-gamma receptor III (Fc-gamma RIII) by aggregated IgG can activate NKT cells and promote disease. The authors showed that the only Fc-gamma receptor expressed by NKT cells is Fc-gamma RIII and that stimulation of NKT cells through this receptor using aggregated IgG was sufficient to activate the cells. Importantly, wild-type NKT cells, but not NKT cells lacking Fc-gamma RIII, mediated antibody-induced joint inflammation when transferred to mice lacking NKT cells and the ability to stimulate NKT cells through their TCR. The demonstration in this study that NKT cells can be activated by stimulation through Fc-gamma RIII alone should impact approaches for the treatment of autoantibody-induced joint inflammation.



TITLE: Fc-gamma RIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation



AUTHOR CONTACT:


Doo Hyun Chung

Seoul National University College of Medicine

Seoul, Republic of Korea

E-mail: doohyunplaza.snu.ac.kr



View the PDF of this article at: AUTOIMMUNITY







JCI table of contents: August 17, 2006



Contact: Karen Honey


Journal of Clinical Investigation


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