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Cells
Volume 12
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10.3390/cells12091229
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Article

Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells

by
Monika Adori
1,
Sharesta Khoenkhoen
1,
Jingdian Zhang
2,
Xaquin Castro Dopico
1 and
Gunilla B. Karlsson Hedestam
1,*
1
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden
2
Department of Medical Biochemistry and Biophysics, Division of Molecular Metabolism and Karolinska Institutet, 171 77 Stockholm, Sweden
*
Author to whom correspondence should be addressed.
Cells 2023, 12(9), 1229; https://doi.org/10.3390/cells12091229
Submission received: 1 March 2023 / Revised: 10 April 2023 / Accepted: 20 April 2023 / Published: 24 April 2023
(This article belongs to the Special Issue Emerging Mechanisms in B Cell Activation)
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Abstract

Lipopolysaccharide (LPS) stimulates dual receptor signaling by bridging the B cell receptor and Toll-like receptor 4 (BCR/TLR4). B cells from IκBNS-deficient bumble mice treated with LPS display reduced proliferative capacity and impaired plasma cell differentiation. To improve our understanding of the regulatory role of IκBNS in B cell activation and differentiation, we investigated the BCR and TLR4 signaling pathways separately by using dimeric anti-IgM Fab (F(ab’)2) or lipid A, respectively. IκBNS-deficient B cells exhibited reduced survival and defective proliferative capacity in response to lipid A compared to B cells from wildtype (wt) control mice. In contrast, anti-IgM stimulation of bumble B cells resulted in enhanced viability and increased differentiation into CD138+ cells compared to control B cells. Anti-IgM-stimulated IκBNS-deficient B cells also showed enhanced cycle progression with increased levels of c-Myc and cyclin D2, and augmented levels of pCD79a, pSyk, and pERK compared to control B cells. These results suggest that IκBNS acts as a negative regulator of BCR signaling and a positive regulator of TLR4 signaling in mouse B cells.
Keywords: nfkbid; NF-κB; IκBNS; B cell activation; B cell receptor; TLR4; LPS; Lipid A; proliferation; cell cycling nfkbid; NF-κB; IκBNS; B cell activation; B cell receptor; TLR4; LPS; Lipid A; proliferation; cell cycling

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MDPI and ACS Style

Adori, M.; Khoenkhoen, S.; Zhang, J.; Dopico, X.C.; Karlsson Hedestam, G.B. Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells. Cells 2023, 12, 1229. https://doi.org/10.3390/cells12091229

AMA Style

Adori M, Khoenkhoen S, Zhang J, Dopico XC, Karlsson Hedestam GB. Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells. Cells. 2023; 12(9):1229. https://doi.org/10.3390/cells12091229

Chicago/Turabian Style

Adori, Monika, Sharesta Khoenkhoen, Jingdian Zhang, Xaquin Castro Dopico, and Gunilla B. Karlsson Hedestam. 2023. "Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells" Cells 12, no. 9: 1229. https://doi.org/10.3390/cells12091229

APA Style

Adori, M., Khoenkhoen, S., Zhang, J., Dopico, X. C., & Karlsson Hedestam, G. B. (2023). Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IκBNS-Deficient B Cells. Cells, 12(9), 1229. https://doi.org/10.3390/cells12091229

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