Activation-Dependent Expression of Low Affinity IgG Receptors FcγRII(CD32) and FcγRIII(CD16) in Subpopulations of Human T Lymphocytes

Engelhardt, Waltraud; Matzke, Jutta; Schmidt, Reinhold

doi:10.1016/s0171-2985(11)80172-5

Cited by 31 publications

(32 citation statements)

References 35 publications

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“…Fcγ RII and Fcγ RIII mRNAs are expressed on phagocytic cells and neutrophils (28,29). Both Fcγ RII and Fcγ RIII have the binding ability to IgG with a low affinity (30). Our study documented that there are two kinds of receptors with different binding affinities on the membrane of HSCs, consistent with the expression of three Fcγ R mRNAs on HSCs.…”

Section: Discussionsupporting

confidence: 79%

Expression of Fc Fragment Receptors of Immunoglobulin G (Fc?Rs) in Rat Hepatic Stellate Cells

et al. 2005

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Hepatic stellate cells (HSCs) are now considered the major cell type in the liver mediating the development of liver fibrosis. Recently it was demonstrated that HSCs express membrane proteins involved in antigen presentation. We further evaluate immunological properties of HSCs by examining the expression and function of the Fc fragment of immunoglobulin G (IgG) in HSCs. In this study, we document the presence of mRNAs for three Fc gammaRs in HSCs. Ligand binding assay indicated the existence of Fc gammaRs with different binding affinities on membranes of HSCs. We also documented that the abundance of the three Fc gammaR mRNAs increased upon activation of HSCs in vitro. Moreover, an examination of the biological activities of IgG revealed that exposure to IgG significantly stimulated HSC differentiation and proliferation. Furthermore, we studied the intracellular signaling protein, LcK, in HSCs and regulation of Lck expression and phosphorylation by IgG. Although IgG did not regulate Lck abundance and phosphorylation in HSCs, highly phosphorylated Lck was present in these cells. In conclusion, we provided evidence that HSCs expresses receptors for the Fc fragment of IgG, and IgG regulates HSC differentiation and proliferation. Therefore, immunoglobulin G may play a role in HSC activation.

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Section: Discussionsupporting

confidence: 79%

Expression of Fc Fragment Receptors of Immunoglobulin G (Fc?Rs) in Rat Hepatic Stellate Cells

et al. 2005

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“…+ FcgRIII + T cells show proliferation in response to receptor cross-linking with ICs [36]. We also observed proliferation of naive CD4 + T cells in response to ICs in the presence of TCC [26].…”

Section: Cd4supporting

confidence: 64%

Immune complexes and late complement proteins trigger activation of Syk tyrosine kinase in human CD4+ T cells

Chauhan

Moore

2012

Clinical and Experimental Immunology

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“…A previous study has also demonstrated IgG binding to as much as 20% of T cells (46). Since most of commercial IgG preparations (typically the Cohn fraction V) are contaminated with the aggregated globulin, we believe that in this study aggregated IgG contributed to the observed binding (46 (42). A total of 3 to 5% CD4 ϩ T-cells expressed CD16 and this population did not increase in response to immobilized IgG (42).…”

Section: Discussionsupporting

confidence: 53%

“…ϩ T-cells express low affinity ϩ T-cells, their role in T-cell mediated immune responses has been largely ignored (15,17,41,42). We observed a co-staining of ICs with the CD3 complex on CD4…”

Section: Discussionmentioning

confidence: 76%

Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

Chauhan

Chen

Moore

et al. 2015

Journal of Biological Chemistry

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Activation-Dependent Expression of Low Affinity IgG Receptors FcγRII(CD32) and FcγRIII(CD16) in Subpopulations of Human T Lymphocytes

Cited by 31 publications

References 35 publications

Expression of Fc Fragment Receptors of Immunoglobulin G (Fc?Rs) in Rat Hepatic Stellate Cells

Expression of Fc Fragment Receptors of Immunoglobulin G (Fc?Rs) in Rat Hepatic Stellate Cells

Immune complexes and late complement proteins trigger activation of Syk tyrosine kinase in human CD4+ T cells

Induced Expression of FcγRIIIa (CD16a) on CD4+ T Cells Triggers Generation of IFN-γhigh Subset

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