This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Topic Collections  • Genetic Counseling/ Testing/ Therapy  • Rheumatology, Other  • Immunologic Disorders  • Dermatology  • Connective Tissue Diseases  • Alert me on articles by topic

Bridget M. Kuehn

JAMA. 2005;293:1315.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Restoring the levels of a receptor coded by a single "gatekeeper" gene can halt the development of lupus in mice, an achievement that may point the way to new therapies targeting the autoimmune disease. The findings, by scientists at Rockefeller University in New York, were published in a pair of articles in January (Fukuyama et al. Nat Immunol. 2005;6:99-106 and McGaha et al. Science. 2005;307:590-593).

The researchers first identified an inhibitory Fc receptor, which is coded by a single gene, that plays a critical role in the ability of the immune system to distinguish between self and nonself in the mouse. They then found that even partial restoration of the receptor’s function prevented the development of lupus in several lupus-prone mouse strains.

Jeffrey V. Ravetch, MD, PhD, head of the university’s Leonard Wagner Laboratory of Molecular Genetics and Immunology, said the findings suggest that even though . . . [Full Text of this Article]