Cell Surface Recycling of Internalized Antigen Permits Dendritic Cell Priming of B Cells

Bergtold, Amy; Desai, Divyakant; Gavhane, Anamika; Clynes, Raphael

doi:10.1016/j.immuni.2005.09.013

Cited by 334 publications

(280 citation statements)

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“…Similarly, there was no significant difference in the expression levels of Fc␥RIIb on CD14 ϩ monocytes and neutrophils between normal controls and active SLE patients despite an increased expression of Fc␥RIa (CD64) on monocytes (data not shown) as previously described (50). (12,13). In each model, the data strongly suggest that Fc␥RIIb is critical for the modulation of immune responses.…”

Section: Comparison Of Fc␥riib Expression Levels On Myeloid-lineage Cmentioning

confidence: 89%

“…Although interfering with the signals mediated by Fc␥RIIb may lead to enhanced myeloid DC (mDC) maturation and immunogenicity (9 -11), several studies suggest that Fc␥RIIb on DCs promotes T-independent humoral responses by presenting native Ag to B cells, and that Fc␥RIIb on follicular DCs facilitates B cell recall responses (12,13). Thus, Fc␥RIIb may have multiple effects on immune function, each of which points to an important role in immune regulation.…”

Section: T He Only Inhibitory Igg Fcr In the Classical Fcr Family (1mentioning

confidence: 99%

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Expression Profile of FcγRIIb on Leukocytes and Its Dysregulation in Systemic Lupus Erythematosus

Yang

et al. 2007

The Journal of Immunology

165

150

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FcγRIIb (CD32B, Online Mendelian Inheritance in Man 604590), an IgG FcR with a tyrosine-based inhibitory motif, plays a critical role in the balance of tolerance and autoimmunity in murine models. However, the high degree of homology between FcγRIIb and FcγRIIa in humans and the lack of specific Abs to differentiate them have hampered study of the normal expression profile of FcγRIIb and its potential dysregulation in autoimmune diseases such as systemic lupus erythematosus (SLE). Using our newly developed anti-FcγRIIb mAb 4F5 which does not react with FcγRIIa, we found that FcγRIIb is expressed on the cell surface of circulating B lymphocytes, monocytes, neutrophils, myeloid dendritic cells (DCs), and at very low levels on plasmacytoid DCs from some donors. Normal donors with the less frequent 2B.4 promoter haplotype have higher FcγRIIb expression on monocytes, neutrophils, and myeloid DCs similar to that reported for B lymphocytes, indicating that FcγRIIb expression on both myeloid and lymphoid cells is regulated by the naturally occurring regulatory single nucleotide polymorphisms in the FCGR2B promoter. FcγRIIb expression in normal controls is up-regulated on memory B lymphocytes compared with naive B lymphocytes. In contrast, in active SLE, FcγRIIb is significantly down-regulated on both memory and plasma B lymphocytes compared with naive and memory/plasma B lymphocytes from normals. Similar down-regulation of FcγRIIb on myeloid-lineage cells in SLE was not seen. Our studies demonstrate the constitutive regulation of FcγRIIb by natural gene polymorphisms and the acquired dysregulation in SLE autoimmunity, which may identify opportunities for using this receptor as a therapeutic target.

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Section: Comparison Of Fc␥riib Expression Levels On Myeloid-lineage Cmentioning

confidence: 89%

Section: T He Only Inhibitory Igg Fcr In the Classical Fcr Family (1mentioning

confidence: 99%

Expression Profile of FcγRIIb on Leukocytes and Its Dysregulation in Systemic Lupus Erythematosus

Yang

et al. 2007

The Journal of Immunology

165

150

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“…Inflammation enhances the stiffness and contractility of APCs through changes in their actomyosin cytoskeleton 149,151 and the active recycling of antigens by APCs suggests that they may also mechanically respond to B cell contacts 152,153 .…”

Section: [H1] Cytoskeletal Regulation Of Biomechanicsmentioning

confidence: 99%

Cytoskeletal control of B cell responses to antigens

Tolar

2017

Nat Rev Immunol

123

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The actin cytoskeleton is essential for cell mechanics and has increasingly been implicated in the regulation of cell signalling. In B cells, the actin cytoskeleton couples extensively to B cell receptor (BCR) signalling pathways and its defects can either enhance or suppress B cell activation. Recent insights from single-cell imaging and biophysical techniques suggest that actin orchestrates BCR signalling at the plasma membrane through effects on protein diffusion, and that it regulates antigen discrimination through the biomechanics of immune synapses. These mechanical functions also play a role in the adaptation of B cell subsets to specialized tasks during antibody responses.3

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“…This mechanism is described to allow the recirculation of antigens to the cell surface, the direct interaction with the BCR and, therefore, the activation of B cells, resulting in the amplification of B cell responses against microbial antigens and autoantigens. 20 B7 mAb displays some properties of the so-called natural antibodies, as multispecificity and idiotypic connectivity. 15 However, this antibody seems to be the result of an antigendriven maturation process, 9 for which a physiological role of this immunopotentiating activity is difficult to postulate.…”

Section: Acknowledgmentsmentioning

confidence: 99%