Comparative studies of lens and retina regeneration have been conducted within a wide variety of animals over the last 100 years. Although amphibians, fish, birds and mammals have all been noted to possess lens- or retina-regenerative properties at specific developmental stages, lens or retina regeneration in adult animals is limited to lower vertebrates. The present review covers the newest perspectives on lens and retina regeneration from these different model organisms with a focus on future trends in regeneration research.
These data indicate that elevated levels of autotaxin and soluble markers of immune activation during HCV infection are partially reversible within 6 months of initiating interferon-free HCV treatment and that autotaxin may be causally linked to immune activation during HCV infection and HCV-HIV coinfection.
During HCV and HIV infection markers of systemic inflammation reflect immune dysfunction as demonstrated by poor response to HAV/HBV neo-antigen vaccine.
We previously showed that human beta defensin-3 (hBD-3) activates mDC via TLR1/2. Here we investigated the effects of hBD-3 on NK cell activation state and effector functions. We observed that hBD-3 activates PBMC to secrete IFN-γ and kill K562 and HUH hepatoma target cells in an NK dependent fashion, and both TLR1/2 and CCR2 are involved. TLR1, TLR2 and CCR2 were expressed on NK cells, and in purified NK culture experiments we observed hBD-3 to directly act on NK cells, resulting in CD69 upregulation and IFNγ secretion. We also observed mDC-hBD-3 enhanced NK cytolytic activity and IFNγ production. These results implicate hBD-3 in its ability to directly activate NK cells and increase NK cell effector function, as well as promote mDC-dependent NK activity. HBD-3 may therefore act as a mediator of innate cell interactions that result in bridging of innate and adaptive immunity.
These data indicate that during chronic HCV infection, race-associated increase in NCR expression and IL28B-associated cytolytic activity may participate in host response to IFN-α-containing HCV therapy.
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