For several years, researchers at Duke University Medical School and Mount Sinai School of Medicine have been trying to understand the role that prothymosin-alpha, a molecule generated by CD8+ T cells, plays in blocking HIV viral replication in virally-infected cells. They've just published a new paper revealing what they believe is the mechanism by which prothymosin-alpha accomplishes this anti-HIV response.
CD8+ T cells, which can have potent anti-HIV activity, produce prothymosin-alpha which then binds to TLR4, a common pattern recognition receptor found on the surface of numerous immune cells and is typically associated with lipopolysaccharide (LPS) recognition to initiate immune responses against gram-negative bacteria. Binding of prothymosin-alpha to TLR4 in macrophages induces production of type I interferons, cytokines famous for their anti-viral capacities.
Such research is interesting for two main reasons. Firstly, we see a novel mechanism by which cells of the adaptive immune system, CD8+ T cells, can induce an anti-viral response via interaction with the innate immune system, i.e. the TLR4 signaling and production of interferons in macrophages. Secondly, this indicates to us that there are naturally occurring molecules produced by immune cells in the body that have anti-HIV activity, and such a discovery could potentially lead to very beneficial therapeutic research.
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