The role of Siglec-G on B cells in autoimmune disease and leukemia

B-cell activation is triggered by the B-cell receptor, but is also controlled by inhibitory receptors, which limit the BCR signaling. CD22 (Siglec-2) and Siglec-G are such inhibitory receptors expressed on B cells. CD22- or Siglec-G deficient mice show enhanced B cell activation.

It was the objective of our study to investigate the role of these inhibitory receptors in autoimmune disease and leukemia.

Ageing Siglec-G deficient or CD22 x Siglec-G deficient mice develop an SLE-like autoimmune disease with autoantibodies and kidney nephritis. In a mouse model for chronic lymphocytic leukemia (CLL), Siglec-G deficient mice show an earlier and more severe disease.

These results show that Siglec-G and CD22 are both involved in preventing autoimmune diseases and leukemia delevopment and could therefore be attractive new targets.