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The cover shows purine P2X7 receptors (red) in spinal cord motor neurons (blue) stained for the neuronal antigen MAP-2 and counterstained with a nuclear marker (DAPI, dark blue/black). On page 821 of this issue, Wang et al. show that blocking these receptors after spinal cord injury improved functional recovery, supported neuronal survival and diminished cell death around the area of the lesion. Magnification, x100.
Research groups worldwide are trying to make immunogens intended to elicit neutralizing antibody responses as part of a prophylactic vaccine to counter the spread of HIV-1. The relative merits of different designs can only be gauged properly through comparative studies, and particularly by evaluating human or animal antisera under identical, or comparable, conditions. Hence there is a need for assay standardization and for the creation of a centralized testing facility that could distribute consensus protocols and reagents.
RNA interference in the brain inhibits neurodegeneration in a polyglutamine disease, SCA1. Is this now the way forward for the clinical treatment of certain genetic disorders (pages 816–820)?
Can tumor progression be understood in terms of the redeployment of mechanisms used in embryonic development? The identification of Twist, a bHLH transcription factor, as a protein linked to metastases in breast cancers would suggest so.
The cytoplasmic protein TRIM5α blocks the growth of HIV in rhesus monkey cells. Three studies now show that TRIM5α is an even more broadly active inhibitor. It impairs the growth of highly divergent retroviruses in human and other primate cells and fully accounts for many previously described antiretroviral activities.
Staphylococcal pneumonia is associated with a huge influx of inflammatory cells into the lungs. A major trigger for this event is now revealed. Protein A, a bacterial surface protein, binds the receptor for TNFα, a prominent activator of the innate immune system (pages 842–848).
For gene therapy of muscular dystrophies, all of the skeletal muscles in the body must be transduced—a tough challenge. An approach that permeabilizes blood vessels using VEGF, helping low doses of a parvovirus-based gene therapy vector sneak across the vessel wall, now solves this problem in mice (pages 828–834).
Two new approaches prevent disease in a model of type 1 diabetes. One approach blocks an activation receptor on disease-conferring T cells. The second deploys suppressor T cells renowned for their ability to inhibit the local immune response.
When the tyrosine kinase inhibitor imatinib (Gleevec) was found to induce high remission rates in patients with chronic myeloid leukemia, this was hailed as a success for targeted tumor therapy. Since then, the repertoire of cancer types that respond to such inhibitors has expanded and researchers are beginning to grapple with the problem of acquired drug resistance. The activating kinase mutations targeted by these drugs can be viewed as the Achilles heel of cancer—they promote malignant progression, yet can turn cancer into a therapeutically exploitable disease.