B cells provide protective immunity by secreting antibodies. When a B cell encounters its specific antigen, B-cell receptor (BCR) signaling initiates actin remodeling. This allows B cells to spread on antigen-bearing surfaces and find more antigen, which increases BCR signaling and facilitates B cell activation. The BCR activates multiple signaling pathways that target actin-regulatory proteins. Although the extracellular signal-regulated kinases ERK1 and ERK2 regulate actin-dependent processes in adherent cells, their role in BCR-induced actin remodeling had not been investigated. Here, we show that targeting ERK with chemical inhibitors or siRNA inhibits BCR-induced spreading in a murine B cell line.
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http://dx.doi.org/10.17912/micropub.biology.000665 | DOI Listing |
Int Immunopharmacol
January 2025
Department of General Surgery, Huashan Hospital, Fudan University, Shanghai 200040 China. Electronic address:
Exosomes derived from cancer cells significantly influence the tumor immune microenvironment and can limit the efficacy of immunotherapy. However, the impact of exosomes on B cell-dependent anti-tumor immunity remains poorly understood. Here, we demonstrate that exosomes secreted by MC38 (MC38-Exos), a murine colorectal cancer cell line, induce B cells to adopt immunosuppressive phenotypes.
View Article and Find Full Text PDFFront Immunol
January 2025
State Key Laboratory of Membrane Biology, School of Life Sciences, Tsinghua-Peking Center for Life Sciences, Institute for Immunology, China Ministry of Education Key Laboratory of Protein Sciences, Beijing, China.
Breast Cancer Res
January 2025
Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Background: CDK4/6 inhibitors have significantly improved the survival of patients with HR-positive/HER2-negative breast cancer, becoming a first-line treatment option. However, the development of resistance to these inhibitors is inevitable. To address this challenge, novel strategies are required to overcome resistance, necessitating a deeper understanding of its mechanisms.
View Article and Find Full Text PDFImmunology
January 2025
Department of Clinical Immunology, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Puducherry, India.
Mechanisms contributing to non-response to treatment in lupus nephritis (LN) are unclear. We characterised the transcriptome of paired peripheral blood mononuclear cells (PBMCs) and renal tissues in LN before and after cyclophosphamide (CYC) treatment and identified markers that predicted treatment response. Total RNA isolated from paired PBMCs (n = 32) and renal tissues (n = 25) of 16 proliferative LN before CYC treatment, 6 months post-treatment, and during renal flare, was sequenced on Illumina Novaseq-6000 platform.
View Article and Find Full Text PDFLAIR1 is an inhibitory receptor broadly expressed on human immune cells, including B cells. LAIR1 has been shown to modulate BCR signaling, however, it is still unclear whether its suppressive activity can be a negative regulator for autoreactivity. In this study, we demonstrate the LAIR1 expression profile on human B cells and prove its regulatory function and relationships to B cell autoreactivity.
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