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Inhibitory CD32b receptors on B cells are critical for humoral immunity. The humoral response plays a role in the pathogenesis of Hashimoto's thyroiditis (HT). This study aimed to investigate B cell subset distribution and CD32b expression within these subsets in HT patients. B cell subset distribution and CD32b expression were analyzed in 60 HT patients and 21 healthy donors. Subset distribution and CD32b expression following stimulation with α-Ig and α-CD40 were also assessed. The percentage of double-negative (DN) memory cells was increased in the HT patients, while the expression level of CD32b on DN memory cells was decreased. Redistribution of B cell subsets was detected in response to stimulation with α-Ig. In addition, the expression level of CD32b was reduced following α-CD40 stimulation. These results suggest that abnormal B cell subset distribution and decreased CD32b expression on DN memory cells might be involved in the pathogenesis of HT.
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http://dx.doi.org/10.1016/j.mce.2016.11.004 | DOI Listing |
Front Immunol
June 2025
Institute of Virology, University Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Introduction: The pentameric C-reactive protein (pCRP), an acute-phase protein, binds to lysophosphatidylcholine (LPC) displayed on the surface of dying cells and microorganisms to activate the complement system and to opsonize immune cells via Fcγ-receptors (FcγRs). Members of the FcγR family are characterized by the recognition of the Fc part of IgG antibodies.
Methods: We utilized a mouse thymoma BW5147 reporter cell panel stably expressing chimeric human FcγR-CD3ζ-chain receptors to define the molecular requirements for FcγR crosslinking by C-reactive protein (CRP).
J Immunol
August 2025
Antibody & Vaccine Group, Centre for Cancer Immunology, School of Cancer Sciences, Faculty of Medicine, Southampton General Hospital, University of Southampton, Southampton, United Kingdom.
The inhibitory Fc gamma receptor IIB (FcγRIIB) is a critical determinant of humoral immunity. By providing feedback inhibition, through inhibitory signalling or competition for antibody Fc engagement, it counterbalances and contextualises cellular responses to signals emanating from co-ligated activating receptors, such as the B-cell receptor and activating FcγR. These activities collectively suppress the emergence of B- cell-mediated autoimmune disease and immune complex-mediated pathologies.
View Article and Find Full Text PDFWhile the inhibitory receptor FcγRIIB has been shown to be upregulated on activated CD8+ T cells in both mice and humans, its effect on T cell fate during infection has not been fully elucidated. We identified an increase in FcγRIIB-expressing CD8+ T cells in patients with COVID-19 relative to healthy controls as well as in mouse models of viral infection. Despite its well-known role as an Fc receptor, FcγRIIB also ligates the immunosuppressive cytokine Fgl2, resulting in CD8+ T cell apoptosis.
View Article and Find Full Text PDFJCI Insight
March 2025
Cancer Biology PhD program.
Cancer immunotherapy has emerged as a promising therapeutic modality but heterogeneity in patient responsiveness remains. Thus, greater understanding of the immunologic factors that dictate response to immunotherapy is critical to improve patient outcomes. Here, we show that fibrinogen-like protein 2 (Fgl2) is elevated in the setting of melanoma in humans and mice and plays a functional role in inhibiting the CD8+ T cell response.
View Article and Find Full Text PDFJ Leukoc Biol
April 2025
Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Apdo. Postal 70228, Ciudad Universitaria, Ciudad de México 04510, Mexico.
Receptors for FcγR on human neutrophils constitute an important mechanism for the recognition of opsonized microorganisms and for cell activation. Human neutrophils express 2 FcγR: FcγRIIa and FcγRIIIb. Previously, it has been reported that activation of each FcγR induces different neutrophil responses by triggering distinct signal transduction pathways, although what particular signal transduction pathway is triggered by each FcγR has not been completely elucidated.
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