Signaling Lymphocytic Activation Molecule Family Member 1 Engagement Inhibits T Cell–B Cell Interaction and Diminishes Interleukin‐6 Production and Plasmablast Differentiation in Systemic Lupus Erythematosus

Objective Signaling lymphocytic activation molecule family member 1 ( SLAMF 1) homophilic interactions promote immunoglobulin production and T cell–B cell cross‐talk. SLAMF 1 is overexpressed on T and B cells in patients with systemic lupus erythematosus ( SLE ). This study was undertaken to determine the role of SLAMF 1 monoclonal antibody ( mA b) in modulating T cell–B cell interaction and B cell activation. Methods Anti‐IgM–prestimulated naive or total B cells from either healthy donors or patients with SLE were cocultured with autologous T cells under CD 3/ CD 28 stimulation, in the presence or absence of the SLAMF 1 mA b. Naive B cells were stimulated with anti‐IgM and CD 40L in the presence of the SLAMF 1 antibody. Cytokine production by CD 4+ T cells and B cells was examined by flow cytometry and/or quantitative polymerase chain reaction. Plasmablast formation and T cell and B cell conjugates were assessed by flow cytometry. IgG and antinuclear antibody production was determined by enzyme‐linked immunosorbent assay. Results SLAMF 1 ligation in a human peripheral blood T cell–B cell culture system reduced the following in both healthy controls and patients with SLE : conjugate formation, interleukin‐6 ( IL ‐6) production by B cells, IL ‐21 and IL ‐17A production by T cells, and Ig and autoantibody production. Whereas the SLAMF 1 mA b directly affected the function of isolated peripheral B cells by decreasing IL ‐6 and Ig production in vitro, it did not affect cytokine production by isolated T cells stimulated in vitro. Conclusion The SLAMF 1 antibody inhibits T cell–B cell interaction and suppresses B cell cytokine production and differentiation, thereby acting as a potential therapeutic tool in the treatment of patients with SLE .