Publications by authors named "Laura Conter"

Both B cell receptor (BCR) and CD40 signaling are rewired in germinal center (GC) B cells (GCBCs) to synergistically induce c-MYC and phosphorylated S6 ribosomal protein (p-S6), markers of positive selection. How interleukin-21 (IL-21), a key T follicular helper (T)-derived cytokine, affects GCBCs is unclear. Like BCR and CD40 signals, IL-21 receptor (IL-21R) plus CD40 signals also synergize to induce c-MYC and p-S6 in GCBCs.

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Memory B cells (MBCs) protect the body from recurring infections. MBCs differ from their naive counterparts (NBCs) in many ways, but functional and surface marker differences are poorly characterized. In addition, although mice are the prevalent model for human immunology, information is limited concerning the nature of homology in B cell compartments.

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In response to T-dependent Ag, germinal centers (GC) generate bone marrow-resident plasma cells (BMPC) and memory B cells (MBC). In this study, we demonstrate that the bone morphogenetic protein receptor 1A (BMPR1A) signaling pathway, which regulates differentiation and self-renewal in multiple stem cell populations, regulates GC dynamics and resultant establishment of BMPC and MBC. Expression studies using quantitative PCR and novel IRES.

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Optimal vaccines are needed for sustained suppression of SARS-CoV-2 and other novel coronaviruses. Here, we developed a recombinant type 5 adenovirus vector encoding the gene for the SARS-CoV-2 S1 subunit antigen (Ad5.SARS-CoV-2-S1) for COVID-19 immunization and evaluated its immunogenicity in mice.

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Germinal center B cells (GCBCs) are critical for generating long-lived humoral immunity. How GCBCs meet the energetic challenge of rapid proliferation is poorly understood. Dividing lymphocytes typically rely on aerobic glycolysis over oxidative phosphorylation for energy.

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Article Synopsis
  • B cell antigen receptor (BCR) signaling is modified in germinal center B cells (GCBCs) to favor the selection of high-affinity B cells, but the specifics of this process are not completely clear.* -
  • A negative feedback loop driven by AKT kinase reduces BCR signaling in GCBCs, which is influenced by changes in phosphorylation and the activity of specific proteins that inhibit BCR signaling.* -
  • Inhibition of AKT can relieve this feedback mechanism, leading to increased activity of key signaling molecules associated with BCR, suggesting a potential pathway for enhancing B cell responses.*
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Article Synopsis
  • CD73 is an enzyme that converts extracellular nucleosides to adenosine, influencing inflammation and T cell activity, and is found in higher amounts on memory B cells but its exact role was previously unclear.
  • The study shows that CD73 levels increase on germinal center B cells after immunization and are very high in T follicular helper cells, but absent in plasma cells and plasmablasts.
  • CD73 knockout mice exhibited a decrease in bone marrow plasma cells later in the immune response, indicating that CD73 is needed for effective plasma cell generation and pointing to its important role in the immune response.
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