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The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish its impact on FoxO transcription factors highlight the AKT-FoxO axis as an on-off switch for MZ B cell formation in mice. In humans, splenic immunoglobulin (Ig) DCD27 B cells, proposed as an MZ B cell equivalent, display higher AKT signaling than naive IgDCD27 and memory IgDCD27 B cells and develop in an AKT-dependent manner from their precursors in vitro, underlining the conservation of this developmental pathway. Consistently, CD148 is identified as a receptor indicative of the level of AKT signaling in B cells, expressed at a higher level in MZ B cells than FO B cells in mice as well as humans.
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http://dx.doi.org/10.1016/j.celrep.2023.112378 | DOI Listing |
J Cell Sci
September 2025
Department of Human Genetics, Emory University School of Medicine, 615 Michael Street, Suite 301, Atlanta, GA 30322, USA.
ARL13B is a regulatory GTPase enriched in cilia, making it a popular marker for this organelle. Arl13bhnn/hnn mice lack ARL13B expression, die during midgestation, and exhibit defects in ciliogenesis. The R26Arl13b-Fucci2aR biosensor mouse line directs the expression of fluorescently tagged full-length Arl13b cDNA upon Cre recombination.
View Article and Find Full Text PDFDiabetes Metab J
September 2025
Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Diabetic foot ulcer (DFU) represents a challenging complication of diabetes mellitus, characterized by slow healing processes. Protein kinase C delta (PKCδ) has been identified as a significant factor in the pathogenesis of various diabetic complications, including DFU. However, the precise underlying mechanisms remain to be fully elucidated.
View Article and Find Full Text PDFBiol Open
September 2025
Departments of Biochemistry & Medical Genetics, University of Manitoba, Winnipeg, R3T 2N2, Canada.
The GM2 gangliosidoses are lysosomal storage disorders exhibiting a spectrum of neurological phenotypes ranging from childhood death to debilitating adult-onset neurological impairment. To date, no mouse model harbouring a specific human mutation causing GM2 gangliosidosis has been created. We used CRISPR/Cas9 to generate knockin (KI) mice with the common adult-onset Hexa Gly269Ser variant as well as knockout (KO) mice with Hexa mutations expected to cause complete HexA deficiency.
View Article and Find Full Text PDFBMB Rep
September 2025
Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896; Department of R&D, Cutiimunebio Inc., Jeonju 54907, Korea.
Atopic dermatitis (AD) is a chronic dermatological disorder characterized by intense pruritus and eczematous lesions. Repeated topical application of 2,4-dinitrofluorobenzene (DNFB) in NC/Nga mice produces AD-like clinical symptoms that closely resemble human AD. N-Acetyl-L-Alanine (L-NAA), a derivative of L-Alanine, has unknown biological and physiological effects on cutaneous tissue.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
August 2025
Anhui Provincial Key Laboratory of Immunology in Chronic Diseases, Bengbu Medical University, Bengbu 233030, China.
Objectives: To investigate the effect of avitinib for suppressing NLRP3 inflammasome activation and alleviating septic shock and explore the underlying mechanism.
Methods: Mouse bone marrow-derived macrophages (BMDM), human monocytic leukemia cell line THP-1, and peripheral blood mononuclear cells (PBMC) isolated from healthy volunteers were pre-treated with avitinib, followed by activation of the canonical NLRP3 inflammasome using agonists including nigericin, monosodium urate (MSU) crystals, or adenosine triphosphate (ATP). Non-canonical NLRP3 inflammasome activation was induced intracellular transfection of lipopolysaccharide (LPS).