LELAND STANFORD JUNIOR UNIVERSITY, THE
Inflammation is an essential host response to tissue damage and/or infection. While it is largely in the confines of an innate response during its initial stages, in vertebrates, it has evolved to require a T cell cytokine, IL-17, to promote the expansion of neutrophils and monocytes in the bone marrow and their release and recruitment to sites of inflammation. This process focuses and strengthens the inflammatory cascade to the injurious site, starts the resolution program and launches the adaptive immune response. Although Il-17 can be elicited from both ab and gd T cells, our previous experiments suggested that gd T cells are uniquely suited to mount an IL-17 response at the onset of acute inflammation. Indeed, we found that gd T? cells are the major IL-17+ population at the onset of CFA immunization. While the development of IL-17+ ab T cells has been well documented, little is known about how IL-17 is regulated in gd T cells. Furthermore, although deficient ab T response has been noted in mice lacking gd T cells, the possibility that these cells act early in an inflammatory response to affect the priming process has not been explored. We will investigate these areas, which are of fundamental importance in understanding host immune defense.