Functional expression of CD43 on human natural killer cells

Aguado, Enrique; Santamarı́a, Manuel; Gallego, M. Dolores; Peña, José; Molina, Ignacio J.

doi:10.1002/jlb.66.6.923

Cited by 18 publications

(10 citation statements)

References 30 publications

(33 reference statements)

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“…All subjects gave their informed consent under the auspices of the appropriate hospital research and ethics committee. Flow Cytometry Analysis HLA-G1 was measured on monocytes (CD14 ϩ ) by indirect immunofluorescence in a FACSVantage cytometer (BD Biosciences, San Jose, CA, USA) as previously described [8]. Briefly, peripheral blood mononuclear cells were obtained by density gradient centrifugation (Lymphoprep; Nycomed Pharma, Oslo, Norway), and cells were incubated using an anti-HLA-G1 mAb as first antibody (MEM-G/9; EXBIO, Prague, Czech Republic) and allophycocyanin (APC) goat anti-mouse Fab (GAM; Caltag, Cambridge, MA, USA) as second antibody.…”

Section: Materials and Methods Patientsmentioning

confidence: 99%

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

et al. 2007

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Section: Materials and Methods Patientsmentioning

confidence: 99%

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

et al. 2007

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“…CD4 + lymphocyte proliferation assays were performed as previously described 24 . Briefly, CD4 + T cells restimulated with TSST‐1 for 20 days were cultured in flat‐bottomed 96‐well tissue culture plates (Nunc, Roskylde, Denmark; 10 5 cells/well) for 72 h in the presence of either 2 µg/well of HP‐3D9 (anti‐CD94), 2 µg/well of 134591 (anti‐NKG2‐C) or 2 µg/well of an isotype‐matched irrelevant mAb.…”

Section: Methodsmentioning

confidence: 99%

Role for NKG2‐A and NKG2‐C surface receptors in chronic CD4⁺ T‐cell responses

et al. 2004

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SummaryThe participation of CD94 and NKG2 gene family members in the function of NK cells and CD8 + cytolytic cells has recently been addressed in detail. However, the role that these molecules play in the key CD4 + regulatory cells remains largely unexplored. This study has examined the expression and regulation of CD94 and NKG2 genes in purified human peripheral CD4 + cells stimulated with several agents. We found a constitutive expression of NKG2-E in CD94-depleted resting peripheral CD4 + cells, whereas inductions of NKG2-A and NKG2-C required chronic cell activation and occurred after expression of CD94. We found that CD3-mediated stimulation induces the expression of CD94 first by day 5 of culture, followed by NKG2-A by day 15 and finally NKG2-C, which is not detected until 20 days after repeated stimulation. This pattern of gene expression differs sharply from that observed in purified CD8 + T cells, where mRNA from all NKG2 gene family members are detected after 5 days of stimulation. Selective activation of TCR V β 2 -bearing cells with toxic shock syndrome toxin-1 superantigen reveals that mRNA induction of NKG2-A and NKG2-C genes is significantly influenced by the presence of cytokines (IL-10 and TGF-β ) and by the restimulation of the cells. In addition, the occupancy of the CD94/NKG2-A receptor expressed on these superantigen-stimulated CD4 + T lymphocytes abrogates TNF-α and IFN-γ production, whereas NKG2-C enhances production of these cytokines. Taken together our results reveal strict gene regulatory mechanisms for CD94 and NKG2 gene expression on CD4 + cells that are different from those governing the expression of these same genes in CD8 + cells. The results suggest that these genes also participate in chronic CD4 + T-cell responses.

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“…These molecules accumulate at the activating NK cell IS (22,23). Consistent with a role in NK cell activation, engagement of CD43 has been shown to increase NK cell proliferation and NK cytotoxicity by redirected lysis (73,74). Thus, the exclusion of CD43 from the inhibitory NK cell IS could assist inhibition by sequestering signaling molecules such as fyn and lck away from the site of intercellular communication.…”

Section: Hla-c-gfp (%)mentioning

confidence: 95%

The Size of the Synaptic Cleft and Distinct Distributions of Filamentous Actin, Ezrin, CD43, and CD45 at Activating and Inhibitory Human NK Cell Immune Synapses

McCann¹,

Vanherberghen²,

Eleme³

et al. 2003

The Journal of Immunology

109

103

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In this study, we report the organization of cytoskeletal and large transmembrane proteins at the inhibitory and activating NK cell immunological or immune synapse (IS). Filamentous actin accumulates at the activating, but not the inhibitory, NK cell IS. However, surprisingly, ezrin and the associated protein CD43 are excluded from the inhibitory, but not the activating, NK cell IS. This distribution of ezrin and CD43 at the inhibitory NK cell IS is similar to that previously seen at the activating T cell IS. CD45 is also excluded from the inhibitory, but not activating, NK cell IS. In addition, electron microscopy reveals wide and narrow domains across the synaptic cleft. Target cell HLA-C, located by immunogold labeling, clusters where the synaptic cleft spans the size of HLA-C bound to the inhibitory killer Ig-like receptor. These data are consistent with assembly of the NK cell IS involving a combination of cytoskeletal-driven mechanisms and thermodynamics favoring the organization of receptor/ligand pairs according to the size of their extracellular domains.

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Functional expression of CD43 on human natural killer cells

Cited by 18 publications

References 30 publications

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

Role for NKG2‐A and NKG2‐C surface receptors in chronic CD4⁺ T‐cell responses

The Size of the Synaptic Cleft and Distinct Distributions of Filamentous Actin, Ezrin, CD43, and CD45 at Activating and Inhibitory Human NK Cell Immune Synapses

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Functional expression of CD43 on human natural killer cells

Cited by 18 publications

References 30 publications

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

Nucleoside Reverse Transcriptase Inhibitors Are Able and Protease Inhibitors Unable to Induce the Tolerogenic Molecule HLA-G1 on Monocytes From HIV-1 Infected Patients

Role for NKG2‐A and NKG2‐C surface receptors in chronic CD4+ T‐cell responses

The Size of the Synaptic Cleft and Distinct Distributions of Filamentous Actin, Ezrin, CD43, and CD45 at Activating and Inhibitory Human NK Cell Immune Synapses

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Role for NKG2‐A and NKG2‐C surface receptors in chronic CD4⁺ T‐cell responses