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- W4313360042 abstract "Abstract Dual-reactive B cells expressing two different immunoglobulin heavy or light chains are present in both healthy humans and mice. However, a subset of systemic lupus erythematosus patients are enriched for dual-reactive B cells. To study dual-reactive B cells in an autoimmune background we used congenic mice bearing a gene targeted human Cκ allele which allowed for the identification and tracking of dual-κ B cells within a polyclonal B cell repertoire. We previously showed that dual-κ B cells positively correlated with disease progression and were enriched in the plasmablast and memory B cell compartments of lupus-prone MRL/lpr mice. Recent studies showed that T cells play a major role in the enrichment of dual-κ B cells, as MRL/lpr mice deficient in the IL-21 receptor had a significant reduction in total dual-κ B cells. In addition, IL-21 signaling was required for the maximal differentiation of dual-κ B cells into plasmablasts and was essential for the development of dual-κ memory B cells. Dual-κ B cells were shown to significantly upregulate antigen presenting molecules such as MHCII, CD80, and CD86. While dual-κ B cells are enriched for polyreactive B cells, immunization with a T-dependent antigen elicited a similar response between single and dual-κ B cells. However, the addition of TLR9 stimulation amplified the antigen-specific response exclusively in dual-k B cells. Furthermore, in vivo EdU incorporation studies showed that dual-k B cells have a higher proliferation rate than single-κ B cells in the absence of exogenous stimuli. Overall, elucidating the diverse molecular pathways promoting the enrichment of dual-reactive B cells in autoimmunity will allow for the selective targeting of these cells in autoimmune patients." @default.
- W4313360042 created "2023-01-06" @default.
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- W4313360042 date "2017-05-01" @default.
- W4313360042 modified "2023-10-12" @default.
- W4313360042 title "Multiple extrinsic signals are required for the enrichment of dual-reactive B cells in autoimmune mice" @default.
- W4313360042 doi "https://doi.org/10.4049/jimmunol.198.supp.54.5" @default.
- W4313360042 hasPublicationYear "2017" @default.
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