SOCS1 silencing could help enhance vaccines against HIV

Researchers from Baylor College of Medicine have shown that switching off a molecule that helps regulate dendritic cells, specialized white blood cells that activate the immune system, could help the host fight HIV infection.

Increasing evidence suggests the host's immune system plays an important, but insufficient, role in limiting HIV infection. Most attempts to stimulate an immune response to HIV have been disappointing.

Exploiting the potential of dendritic cells to activate the immune system could help scientists develop an effective host response to prevent or control HIV infection, according to the US study.

Si-Yi Chen and colleagues studied a molecule, SOCS1, which regulates how antigens (small parts of proteins from microbes or tumour cells, which trigger an immune response) are handled by dendritic cells. They have previously found that dendritic cells in which the SOCS1 was turned off were more efficient at stimulating others of the body's immune cells.

Now Chen and colleagues have found that in mice SOCS1 is part of a pathway that not only controls the production of compounds (cytokines) that stimulate inflammation but also has a critical role in regulating the anti-HIV immune response. Dendritic cells in which SOCS1 was switched off were able to induce a good memory immune response to HIV. In addition, the potency of HIV DNA vaccination was enhanced by co-immunization with an interfering RNA that switched off SOCS1.

The authors suggest that this SOCS1 silencing strategy could help enhance therapeutic and prophylactic vaccines against HIV and other pathogens.

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