Targeting CD22 with the monoclonal antibody epratuzumab modulates human B-cell maturation and cytokine production in response to Toll-like receptor 7 (TLR7) and B-cell receptor (BCR) signaling.

ABSTRACT:

Background

Abnormal B-cell activation is implicated in the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE). The B-cell surface molecule CD22, which regulates activation through the B-cell receptor (BCR), is a potential target for inhibiting pathogenic B cells; however, the regulatory functions of CD22 remain poorly understood. In this study, we determined how targeting of CD22 with epratuzumab (Emab), a humanized anti-CD22 IgG1 monoclonal antibody, affects the activation of human B-cell subsets in response to Toll-like receptor 7 (TLR7) and BCR engagement.

Methods

B-cell subsets were isolated from human tonsils and stimulated with F(ab')₂ anti-human IgM and/or the TLR7 agonist R848 in the presence of Emab or a human IgG1 isotype c

SUBMITTER: Giltiay NV 

PROVIDER: S-EPMC5433084 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature