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Members of the galectin family of proteins have been shown to regulate the development and the function of immune cells. We previously identified the increased expression of galectin-1 and galectin-3 mRNA and protein in anergic B cells relative to their naïve counterparts. To investigate the role of these galectins in maintaining B cell tolerance, we crossed mice deficient in galectin-1 or galectin-3 with mice bearing a lupus autoantigen-binding transgenic (Tg) B cell receptor, using a model with a well-characterized B cell tolerance phenotype of deletion, receptor editing and anergy. Here, we present data showing that the global knockout of galectin-1 or galectin-3 yields subtle alterations in B cell fate in autoantibody Tg mice. The absence of galectin-3 leads to a significant increase in the number of Tg spleen B cells, with the recovery of anti-laminin antibodies from a subset of mice. The B cell number increases further in antibody Tg mice with the dual deficiency of both galectin-1 and galectin-3. Isolated galectin-1 deficiency significantly enhances the proliferation of Tg B cells in response to lipopolysaccharide stimulation. These findings add to the growing body of evidence indicating a role for the various galectin family members, and for galectins 1 and 3 in particular, in the regulation of autoimmunity.

Lack of galectin-1 or galectin-3 alters B cell deletion and anergy in an autoantibody transgene model