ABSTRACT
Spin interaction in antiferromagnetic materials is of central interest in the recently emerging antiferromagnetic spintronics. In this Letter, we explore the spin current interaction in antiferromagnetic FeMn by the spin pumping effect. Exchange biased FeNi/FeMn films, in which the Néel vector can be presumably controlled via the exchange spring effect, are employed to investigate the damping enhancement depending on the relative orientation between the Néel vector and the polarization of the pumped spin current. The correlation between the enhanced damping and the strength of the exchange bias suggests that the twisting of the Néel vector induces an additional spin dissipation, which verifies that the Slonczewski-type spin torque is effective even in antiferromagnetic materials.
ABSTRACT
IL-17A is originally identified as a proinflammatory cytokine that induces neutrophils. Although IL-17A production by CD4(+) Th17 T cells is well documented, it is not clear whether IL-17A is produced and participates in the innate immune response against infections. In the present report, we demonstrate that IL-17A is expressed in the liver of mice infected with Listeria monocytogenes from an early stage of infection. IL-17A is important in protective immunity at an early stage of listerial infection in the liver because IL-17A-deficient mice showed aggravation of the protective response. The major IL-17A-producing cells at the early stage were TCR gammadelta T cells expressing TCR Vgamma4 or Vgamma6. Interestingly, TCR gammadelta T cells expressing both IFN-gamma and IL-17A were hardly detected, indicating that the IL-17A-producing TCR gammadelta T cells are distinct from IFN-gamma-producing gammadelta T cells, similar to the distinction between Th17 and Th1 in CD4(+) T cells. All the results suggest that IL-17A is a newly discovered effector molecule produced by TCR gammadelta T cells, which is important in innate immunity in the liver.
Subject(s)
Immunity, Innate , Interleukin-17/immunology , Listeriosis/immunology , Liver Diseases/microbiology , Receptors, Antigen, T-Cell, gamma-delta , T-Lymphocytes/immunology , Animals , Interferon-gamma/biosynthesis , Interleukin-17/biosynthesis , Listeria monocytogenes , Mice , Mice, Knockout , T-Lymphocyte Subsets/immunologyABSTRACT
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.
