|
||
J. Exp. Med.,
Volume 189, Number 8, April 19, 1999 1307-1313
By
From the Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH,
United Kingdom
CD22 is a B cell-specific transmembrane glycoprotein that acts to dampen signals generated
through the B cell antigen receptor (BCR): B cells from CD22-deficient mice give increased
Ca2+ fluxes on BCR ligation. Here we show that this B cell hyperresponsiveness correlates
with the development of autoantibodies. After the age of eight months, CD22-deficient mice
developed high titers of serum IgG directed against double-stranded DNA; these antibodies were of multiclonal origin, somatically mutated, and high affinity. Increased titers of antibodies
to cardiolipin and myeloperoxidase were also noted. The results demonstrate that a single gene
defect exclusive to B lymphocytes is, without additional contrivance, sufficient to trigger autoantibody development in a large proportion of aging animals. Thus, CD22 might have evolved
specifically to regulate B cell triggering thresholds for the avoidance of autoimmunity.
This article has been cited by other articles:
| TABLE OF CONTENTS |
|