Northwestern University Medical School scientists cloned andsequenced the receptor genes expressed by pathogenic T cells inlupus, they reported at the American College of Rheumatologymeeting held this week in Minneapolis.Researchers at the medical school in Chicago, led by Syamal Datta,professor of medicine and professor of microbiology andimmunology, found that the anti-DNA antibodies produced bycertain B cells in lupus are pathogenic, or fail to clear the circulatingDNA.The researchers cloned the genes for the anti-DNA autoantibodiesand found they coded for positively charged residues on the antigen-binding sites of the autoantibodies. The positively charged antibodiescause disease, the researchers said, by binding to the negativelycharged sites in the kidneys, joints, blood vessels and other tissues.Dennis Boulware, professor of medicine at the University ofAlabama at Birmingham, told BioWorld that the finding will assistresearchers in designing therapies because of the understanding ofinitial events that lead to the disease."This follows by five to 10 years what happened in rheumatoidarthritis," Boulware said. "Three to five years from now we'll havestudies in humans in lupus, trying to control the disease."We've been treating people at the end of that cascade when all youcan see is inflammation in various parts of the body," he said. "Wehave never understood if lupus is a normal response to somethingdriving the whole immune system, or if the system has suddenlygone crazy by itself."Those receptors responsible for triggering and setting off immunesystem processes are not entirely at random," Boulware said. "Theyseem to be restricted, as if they're made to have this response. If youcan identify the precise level at which that abnormality exists, andhow that reaction is abnormal, then you can design therapies to turnoff that system." n
-- Jim Shrine
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