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

Semin Arthritis Rheum. 2024 Feb:64S:152328. doi: 10.1016/j.semarthrit.2023.152328. Epub 2023 Nov 22.

Abstract

Background: 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.

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

Results: 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.

Author's conclusions: 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.

Keywords: None.

MeSH terms

  • Animals
  • Autoimmune Diseases*
  • Autoimmunity
  • B-Lymphocytes
  • Leukemia*
  • Mice
  • Sialic Acid Binding Immunoglobulin-like Lectins

Substances

  • Sialic Acid Binding Immunoglobulin-like Lectins
  • Siglecg protein, mouse