Researchers at The Scripps Research Institute (TSRI) have discovered a way to stimulate the "immune memory" in mice to prevent or clear a viral infection. Immune memory allows the body to recognize, respond and eliminate viruses after initial exposure and is the principal behind viral vaccines. But not all vaccines are 100 percent effective in conveying immunity.
During an immune response, certain proteins speed the creation of immune cells that target viral infection. At the same time, other proteins moderate this response so that destructive autoimmunity isn't triggered. For example, the immunomodulating agent IL-10 does this by dampening specialized T-cell production. Some viruses have evolved the ability to enhance IL-10 production when invading a host, thus disabling the immune system when needed most and leading to persistent infection.
Researchers achieved an enhanced immune response by engineering mice lacking the genes for IL-10 production. Thus, more immune cells were produced. This enhanced response was also seen in normal mice given antibodies designed to target and block IL-10 production.
The results appear in the Proceedings of the National Academy of Sciences (PNAS). (News release http://bit.ly/bQwoMH.)
Stress tied to alcohol addiction
A stress hormone called corticotropin-releasing factor (CRF) was believed to be involved in alcohol dependence. Following six years of research, scientists from The Scripps Research Institute have confirmed, in an animal model, CRF's central role in alcohol addiction. In addition, the studies showed that blocking the hormone on a long-term basis alleviated the symptoms of alcohol dependence in rats.
CRF is a natural substance involved in the body's stress response. Originally found only in the area of the brain's hypothalamus, it has now been localized in other brain regions, including the amygdala, an area that has been implicated in the elevated anxiety, withdrawal, and excessive drinking associated with alcohol dependence.
The findings will appear in an upcoming edition of the journal Biological Psychiatry. (News release http://bit.ly/affSes.)
Tumors outsmarting drugs
Researchers at the Ludwig Institute for Cancer Research (LICR) at the UCSD School of Medicine and Moores UCSD Cancer Center have shown how a deadly type of brain tumor (gliomas) can evade therapeutic drugs.
Current attempts to halt glioma growth have been aimed at blocking the epidermal growth factor receptor (EGFR); a cell-signaling protein known to be crucial for tumor growth. Researchers created a genetic system in mice that controlled EGFR expression, turning it off and on with the drug tetracycline. They found that tumor growth would stop initially when tetracycline blocked EGFR, but would later resume growing, even without EGFR, meaning something else was driving tumor growth.
Additional studies revealed that a gene called KLHDC8 is over-expressed in gliomas in which the EGFR protein is inhibited. This means that drug therapy needs to target both the EGFR receptor and the KLHDC8 alternate pathway.
The findings appear in the Proceedings of the National Academy of Sciences. (News release http://bit.ly/6kkU1Y.)
Lynne Friedmann is a science writer based in Solana Beach.
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