| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Research Abstract |
Streptococcus pneumoniae is a causative agent of bacterial pneumonia in human. The bacterial cell wall components contain the capsular polysaccharides which play an important role for evading the host immune responses. That is why the antibody specific for capsular polysaccharides is protective against S. pneumoniae infection by inducing the activation of complements system and phagocytosis by macrophages or dendritic cells. Type-I interferons (IFNs) were shown to be induced in response to S. pneumoniae infection, and possibly regulate the bacterial infection. However, it is not clear whether the type-I IFNs affect the antibody production against pneumococcalcapsular polysaccharides from splenic marginal zone B cells. This study revealed the effects of Type-I IFNs against marginal zone B cells for production of IgM specific for pneumococcal capsular polysaccharides
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