Abstract
Murine gammadelta T cells participate in the innate immune response against infection by an intracellular pathogen Listeria monocytogenes. Vdelta1+gammadelta T cells coexpressing Vgamma6 are a major gammadelta T-cell subpopulation induced at an early stage of L. monocytogenes infection in the livers of infected mice. To investigate the protective role of the Vgamma6/Vdelta1+gammadelta T cells against L. monocytogenes infection, Vdelta1 gene-deficient (Vdelta1-/-) mice were analysed because these mice selectively lacked a Vgamma6/Vdelta1+gammadelta T-cell subpopulation in the L. monocytogenes-infected liver. The Vdelta1-/- mice showed increased bacterial burden in the liver and spleen, and decreased survival rate at an early stage of L. monocytogenes infection when compared to wild-type mice. Histological examination showed abscess-like lesions and unorganized distribution of macrophages in the liver of the Vdelta1-/- mice but not in the wild-type mice after L. monocytogenes infection. The Vgamma6/Vdelta1+gammadelta T cells produced interferon-gamma and interleukin-17A. All the results suggest that murine Vgamma6/Vdelta1+gammadelta T cells control the innate protective response against L. monocytogenes infection through production of the proinflammatory cytokines interferon-gamma and interleukin-17A in the infected liver.