| Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2012: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2011: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2010: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
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| Research Abstract |
MHC recognizing receptors expressed on natural killer cells and cytotoxic T cells, KIRs and LILRs, have a pivotal role on regulation of virus infection. The mutation of a HIV-derived peptide on MHC molecule disrupt T cell function and also inhibit NK function by increasing the binding activity of an inhibitory KIR. Here we successfully determined the structure of a LILR-MHC complex at low resolution, revealing that this complex structure is similar to the previously reported LILR-MHC complexes, LILR recognize the site far from the peptide-binding region and thus the HIV peptide mutations do not likely affect the LILR binding, supported by our binding study. On the other hand, we also determined the crystal structure of the MHC class I molecule displaying the HIV mutant peptide, which increased the KIR binding, revealing the molecular mechanism for the change of KIR binding activity.
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