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Autoimmunity

Decoy receptors thwart B cells

Nature volume 404, pages 949–950 (2000) Cite this article

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Lupus erythematosus is a debilitating autoimmune disease. It is characterized by pathological defects in many organs; by hyperactive immune cells called B lymphocytes, secreting self-reactive antibodies; and by a many-gene pattern of inheritance. A new piece to the physiological puzzle of this disease was revealed recently in the shape of a protein — called BAFF — that sends B cells into hyperdrive, leading to a lupus-like syndrome in mice1,2. On page 995 of this issue3, Gross and colleagues define two receptors for this protein. They then use this key insight to construct a specific antagonist for BAFF that can slow the progression of certain features of the disease in autoimmune-prone mice. This work may have opened up a new avenue to the treatment of lupus erythematosus.

Many factors, both environmental and genetic — a lot of which remain ill defined4 — contribute to the onset of lupus erythematosus. Animal models have been instrumental in providing clues to the pathology of autoimmune diseases in humans. For example, the first generation of offspring of the ‘New Zealand B and W’ mouse strains develop a lupus-like syndrome at around eight months of age: they have antibodies that react to their own nuclear molecules, including DNA, and a progressively worsening kidney disease5. The symptoms result in part from the immune-reactive complexes deposited in the networks of blood capillaries in the kidneys, and from the presence of activated B cells, which contribute to the inflammatory milieu. Eventually, kidney failure results — much as in the human disease.

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Figure 1: Lupus erythematosus in a mouse model.
Figure 2: Decoy receptors suppress autoimmune diseases.

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  1. Division of Molecular Immunology La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, 92121 , California, USA

    Carl F. Ware

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  1. Carl F. Ware
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Correspondence to Carl F. Ware.

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Ware, C. Decoy receptors thwart B cells. Nature 404, 949–950 (2000). https://doi.org/10.1038/35010263

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