Editor's Note: Science Scan is a roundup of recently published biotechnology-relevant research.

The genetic blueprint for human life may well turn out to be a drug that can powerfully "trick" a malfunctioning immune system into curing autoimmune disease. Proof of concept for using a "tolerizing" DNA-based pharmaceutical to successfully treat a model of autoimmune disease is reported in the September 2003 issue of Nature Biotechnology. Its title: "Protein microarrays guide tolerizing DNA vaccine treatment of experimental autoimmune encephalomyelitis."

This is an animal model that mimics the features and symptoms of multiple sclerosis. Its purpose is to advance the treatment of MS, and set a foundation for future personalized medicines in which DNA will prove the drug of choice.

For the last 10 to 15 years, most research exploring how the human immune system might be modified to provide a positive therapeutic outcome has focused on the two main aspects of the human immune system. The "innate" aspect marshals an instant first response to foreign substances for the sole purpose of eliminating them. Less attention has been made to the "adaptive" immune response, which helps the body's immune cells develop a "memory" of such invasive attacks, thereby providing long-term protection against future insult.

The journal article yields some startling insight into how that system might be tricked or reprogrammed by DNA-based drugs to help individuals with autoimmune diseases - in particular, MS. The hallmark of an autoimmune disease is mounting a protective immune system response to substances that are neither foreign nor life-threatening, but actually are seen by the immune system as "self." In autoimmunity, the body mounts a defense against its own tissues and cells. It works to destroy or damage such tissues as if they were invaders.

Thus, T-helper-1 cells (T_h1) become aggressive; instead of helping other cells to protect the body, they activate a series of inflammatory events that become tissue destructive. Bayhill Therapeutics Inc., of Palo Alto, Calif., (a co-author of the paper) is designing therapies that will "quiet" or terminate the activities of T_h1 cells in autoimmune diseases.

In MS in particular, Bayhill's goal is to reverse - but not prevent - the inflammation caused by the body's attack on the myelin sheaths of its own nervous system. It also is working to advance research programs in other diseases, including diabetes. With proof of concept in Phase I/II studies in selected diseases, Bayhill expects to expand its approach to a broad range of other autoimmune-mediated diseases such as rheumatoid arthritis and systemic lupus erythematosus.

Dyslexia - Commonest Childhood Learning Disability - Traced To Chemicals In The Brain

Finnish and Swedish molecular geneticists have identified a human gene that is disrupted in some cases of dyslexia - the most common childhood learning disability. Up to 10 percent of people are affected by the condition. It makes reading difficult, without regard to intelligence or education. Previous research established a genetic link to dyslexia and narrowed down the hunt to regions thought to contain loci on several chromosomes.

An article in the Proceedings of the National Academy of Sciences (PNAS), released online Aug. 25-29, bears the title: "A candidate gene for developmental dyslexia encodes a nuclear tetratricopeptide repeat domain protein dynamically regulated in brain." Its co-authors are at the University of Helsinki in Finland and the Karolinska Institute in Stockholm, Sweden.

The co-authors studied individuals from 20 different Finnish families. They compared the genetic makeup of the dyslexic and nondyslexic members of each family, focusing their search on the previously identified target areas. In one family, a gene called DYX1C1 was disrupted. In another, the same gene contained a stop sign in the wrong place, producing a truncated protein. DYX1C1 mutations appeared as a risk factor in other families as well. Analysis of the protein's sequence revealed that it is not similar to any other known proteins. This one is expressed in several tissues but shows up most heavily in the brain. Comparison of DYX1C1 expression in normal brains and those of stroke victims suggests that the protein may be active in regulating brain cells in the face of metabolic stress.

The Bacterium Helicobacter Pylori Threatens More Than Ulcers - Gastric Cancer As Well

The gut pathogen responsible for ulcers and some gastric cancers is found in roughly half the world's population. It directly suppresses immune cells in the stomach, as reported in Science, dated Aug. 22, 2003. The paper is titled "Helicobacter pylori vacuolating cytotoxin inhibits T-lymphocyte activation." Its co-authors are at the Pettenkofer Institute for Microbiology in Munich, Germany.

The pathogen acts by directly suppressing immune cells in the stomach, the article states. The co-authors show that the bacteria blocks the activation and proliferation of T cells. These immune system cells are responsible for killing virus-infected cells and regulating the activities of other white blood cells.

The scientists found that the bacteria secretes a vacuolating cytotoxin, VacA, which targets the T-cell signaling pathway. VacA partially mimicked the activity of the immunosuppressive drug FK506 by possibly inducing a local immune suppression. That would explain the extraordinary chronicity of H. bacter infections. It ultimately disrupts expression of the genes involved in inducing inflammation and controlling an efficient immune response in the stomach. The authors suggest that these findings might explain how the chronic and persistent bacteria are able to infect the human stomach for years, even decades.