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.
Citation: Song XT, Evel-Kabler K, Rollins L, Aldrich M, Gao F, et al. (2006) An alternative and effective HIV vaccination approach based on inhibition of antigen presentation attenuators in dendritic cells. PLoS Med 3(1): e11.
Si-Yi Chen MD. Ph.D.
Baylor College of Medicine
One Baylor Plaza
Houston, TX USA 77030
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