Immunological memory is a composite of lasting antibody titers maintained by plasma cells in conjunction with memory T and B cells. Memory B cells are a critical reservoir for plasma cell generation in the secondary response. Identification of memory B cells requires that they be distinguished from naïve, activated, and germinal center precursors and from plasma cells. Memory B cells are heterogeneous in isotype usage, immunoglobulin mutational content, and phenotypic marker expression. Phenotypic subsets of memory B cells are defined by PD-L2, CD80, and CD73 expression in mice, by CD27 and FCRL4 expression in humans and by T-bet in both mice and humans. These subsets display marked functional heterogeneity, including the ability to rapidly differentiate into plasma cells versus seed germinal centers in the secondary response. Memory B cells are located in the spleen, blood, other lymphoid organs, and barrier tissues, and recent evidence indicates that some memory B cells may be dedicated tissue-resident populations. Open questions about memory B cell longevity, renewal and progenitor-successor relationships with plasma cells are discussed.
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http://dx.doi.org/10.1111/imr.13016 | DOI Listing |
J Am Chem Soc
January 2025
Department of Pharmacy, The First Affiliated Hospital of USTC; Division of Life Sciences and Medicine, University of Science and Technology of China, Anhui Provincial Key Laboratory of Precision Pharmaceutical Preparation and Clinical Pharmacy, Hefei, Anhui 230026, China.
Inhibitors of the PD-1/PD-L1 immune checkpoint have revolutionized cancer treatment. However, the clinical response remains limited, with only 20% of patients benefiting from treatment and approximately 60% of PD-L1-positive patients exhibiting resistance. One key factor contributing to resistance is the externalization of phosphatidylserine (PS) on the surface of cancer cells, which suppresses immune responses and promotes PD-L1 expression, further hindering the efficacy of PD-L1 blockade therapies.
View Article and Find Full Text PDFAllergy
January 2025
Institute for Systemic Inflammation Research, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Nutrients
December 2024
Department of Pharmacognosy with Medicinal Plant Garden, Medical University in Lublin, 1 Chodzki St., 20-093 Lublin, Poland.
: We assessed the influence of long-term injection of magnoflorine (MAG) on memory acquisition in mice for the first time. : This isoquinoline alkaloid that belongs to the aporphines was isolated from the roots of by centrifugal partition chromatography (CPC) using a biphasic solvent system composed of chloroform: methanol: water in the ratio 4:3:3 (//) with 20 mM of hydrochloric acid and triethylamine, within 64 min. : Our results indicated that long-term injection of MAG 20 mg/kg dose improve the long-term memory acquisition in mice that were evaluated in the passive avoidance (PA) test with no toxicity records.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Neuropharmacology Laboratory, The Mina & Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 5290002, Israel.
Chronic cocaine use triggers inflammatory and oxidative processes in the central nervous system, resulting in impaired microglia. Mesenchymal stem cells, known for their immunomodulatory properties, have shown promise in reducing inflammation and enhancing neuronal survival. The study employed the cocaine self-administration model, focusing on ionized calcium-binding adaptor protein 1 (Iba-1) and cell morphology as markers for microglial impairment and PLX-PAD cells as a treatment for attenuating cocaine craving.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Neurology, Davis School of Medicine, University of California, 1515 Newton Court, Davis, CA 95618, USA.
We have designed and produced 39 amino acid peptide mimics of the and human acetylcholine receptors' (AChRs) main immunogenic regions (MIRs). These conformationally sensitive regions consist of three non-contiguous segments of the AChR α-subunits and are the target of 50-70% of the anti-AChR autoantibodies (Abs) in human myasthenic serum and in the serum of rats with a model of that disease, experimental autoimmune myasthenia gravis (EAMG), induced by immunizing the rats with the electric organ AChR. These MIR segments covalently joined together bind a significant fraction of the monoclonal antibodies (mAbs) raised in rats against electric organ AChR.
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