CD22 Promotes B-1b Cell Responses to T Cell-Independent Type 2 Antigens.

ABSTRACT: CD22 (Siglec-2) is a critical regulator of B cell activation and survival. CD22^-/- mice generate significantly impaired Ab responses to T cell-independent type 2 (TI-2) Ags, including haptenated Ficoll and pneumococcal polysaccharides, Ags that elicit poor T cell help and activate BCR signaling via multivalent epitope crosslinking. This has been proposed to be due to impaired marginal zone (MZ) B cell development/maintenance in CD22^-/- mice. However, mice expressing a mutant form of CD22 unable to bind sialic acid ligands generated normal TI-2 Ab responses, despite significantly reduced MZ B cells. Moreover, mice treated with CD22 ligand-binding blocking mAbs, which deplete MZ B cells, had little effect on TI-2 Ab responses. We therefore investigated the effects of CD

SUBMITTER: Haas KM 

PROVIDER: S-EPMC5821584 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature