| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Research Abstract |
CD4 T cell-mediated immune response is essential for the control of M. tuberculosis (Mtb) infection. Recent studies of the programmed cell death 1 (PD-1) receptor have provided novel insights into the inhibition of T-cell activation in infectious diseases. To clarify the role of PD-1 in Mtb infection, I investigated the course of Mtb infection in PD-1 KO mice. After infection, PD-1 KO mice die rapidly owing to severe lung damage. PD-1 KO mice developed higher numbers of IFN-γ-producing CD4 T cells compared to control mice. By using adoptive transfer and antibody blockade experiments, PD-1 deficiency in CD4 T cells and IFN-γ production by CD4 T cells aresufficient to cause the increased susceptibility to infection. These data show that PD-1 is essential in limiting CD4 T cell-mediated pathology in Mtb infection.
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