Innate and adaptive signals enhance differentiation and expansion of dual-antibody autoreactive B cells in lupus

Allison Sang, Thomas Danhorn, Jacob N. Peterson, Andrew L. Rankin, Brian P. O’Connor, Sonia M. Leach, Raul M. Torres and Roberta Pelanda ()
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Allison Sang: University of Colorado School of Medicine
Thomas Danhorn: National Jewish Health
Jacob N. Peterson: University of Colorado School of Medicine
Andrew L. Rankin: Pfizer Research
Brian P. O’Connor: University of Colorado School of Medicine
Sonia M. Leach: National Jewish Health
Raul M. Torres: University of Colorado School of Medicine
Roberta Pelanda: University of Colorado School of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Autoreactive B cells have a major function in autoimmunity. A small subset of B cells expressing two distinct B-cell-antigen-receptors (B2R cells) is elevated in many patients with systematic lupus erythematosus (SLE) and in the MRL(/lpr) mouse model of lupus, and is often autoreactive. Here we show, using RNAseq and in vitro and in vivo analyses, signals that are required for promoting B2R cell numbers and effector function in autoimmune mice. Compared with conventional B cells, B2R cells are more responsive to Toll-like receptor 7/9 and type I/II interferon treatment, display higher levels of MHCII and co-receptors, and depend on IL-21 for their homeostasis; moreover they expand better upon T cell-dependent antigen stimulation, and mount a more robust memory response, which are characteristics essential for enhanced (auto)immune responses. Our findings thus provide insights on the stimuli for the expansion of an autoreactive B cell subset that may contribute to the etiology of SLE.

Date: 2018
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DOI: 10.1038/s41467-018-06293-z

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