Involvement of cyclic AMP and nitric oxide in immunoglobulin E-dependent activation of Fc epsilon RII/CD23+ normal human keratinocytes.

Becherel, Pierre-André; Mossalayi, M. Djavad; Ouaaz, F; Goff, Liliane Le; Dugas, Bernard; Paul‐Eugène, Nathalie; Françès, Camille; Chosidow, Olivier; Kilchherr, Erich; Guillosson, Jean‐Jacques

doi:10.1172/jci117227

Cited by 50 publications

(36 citation statements)

References 23 publications

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“…In addition to its ability to bind IgE (FcεRII), CD23 displays various other physiologic ligands such as CD21, CD11b/c, CD47-vitronectin, and mannose-containing proteins (20,29). CD23 cross-linking by its ligands promotes the secretion of IL-1, IL-6, TNF-␣, superoxide, and NO from various human cells (4,6,29). In the present study, we show that CD23 ligation promotes antimicrobial activity of human macrophages, in part through the generation of NO and TNF-␣, two potent antimycobacterial mediators.…”

Section: Discussionmentioning

confidence: 99%

“…Infected MDM were directly activated through CD23 pathway, while CD23 cell surface expression was induced in uninfected MDM in the presence of 10 ng of recombinant IL-4/ml, as described elsewhere (48). CD23-positive cells were incubated in the presence of cross-linking anti-CD23 monoclonal antibody (anti-CD23 MAb; clone 135, immunoglobulin G1 [IgG1], 20 g/ml; Novartis, Geneva, Switzerland) or human IgE/anti-IgE (10 g of each/ml; Nordic, Tilburg, The Netherlands) immune complexes as detailed elsewhere (6,48). MDM cultures were supplemented with the chemical NO donor, SNAP (S-nitroso-Nacetylpenicillamine; Coger, Paris, France), recombinant human IL-10, TNF-␣, or neutralizing anti-human TNF-␣ (Genzyme, Cambridge, MA).…”

Section: Methodsmentioning

confidence: 99%

“…In human macrophages, CD23 ligation is well known to promote gene expression and the secretion of various inflammatory cytokines, including TNF-␣, IL-1, IL-6, and IL-8, among others (29,35). The CD23 pathway also promotes the generation of superoxide, the transcription of iNOS gene, and subsequent production of NO from human macrophages, eosinophils, and epithelial cells (4,6,48). Since NO mediates microbiostatic effect, we sought to determine whether the NO pathway had a role in the inhibition of M. avium CFU after CD23 activation.…”

Section: Avium Promotes Functional Cd23 Expression By Human Macropmentioning

confidence: 99%

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CD23 Mediates Antimycobacterial Activity of Human Macrophages

et al. 2009

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Avium Promotes Functional Cd23 Expression By Human Macropmentioning

confidence: 99%

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CD23 Mediates Antimycobacterial Activity of Human Macrophages

et al. 2009

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“…Results are the mean ± SD from triplicate cultures. (18)(19)(20)(21). We investigated the role of TNF-a in L. major killing by human macrophages, when these were activated by either CD23 mAb or IFN-,y.…”

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confidence: 99%

The killing of Leishmania major by human macrophages is mediated by nitric oxide induced after ligation of the Fc epsilon RII/CD23 surface antigen.

Vouldoukis

Riveros‐Moreno

Dugas

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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148

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Serum IgE concentrations and the expression of the low-affinity receptor for IgE (FceRHl/CD23) Nitric oxide (NO) generated by activated murine macrophages is cytostatic or cytotoxic for a variety of pathogens, including Leishmania major, Plasmodium falciparum, Schistosoma mansoni, Trypanosoma cruzi, and Toxoplasma gondii (1-6). NO is generated from the oxidation of the terminal guanido nitrogen atom(s) of L-arginine by an NADPH-dependent enzyme, the NO synthase (NOS) (7-9). In murine macrophages, NOS activity is induced by lipopolysaccharide (LPS) (9) IgE-IC) or by a specific monoclonal antibody (mAb) to CD23 (CD23 mAb) promotes the generation of cGMP. Simultaneous measurement of the generation of nitrite (NO-j) indicated that the enhanced production of cGMP is consequent to activation of the L-arginine:NO pathway.The low-affinity receptor for IgE (FceRII/CD23) is also expressed on normal human monocytes/macrophages after their activation in vivo (22,23). Studies in patients infected with Leishmania braziliensis or in disease-free, immunoreactive donors have shown both in situ CD23 expression and serum IgE concentrations to be increased in these conditions (23). We have, therefore, studied whether cell activation through ligation of the membrane receptor CD23 induces the L-arginine:NO pathway and results in leishmanicidal activity in human macrophages. MATERIALS AND METHODSReagents. The following reagents were used: recombinant human interleukin 4 (IL-4; a gift from J. Banchereau, Schering-Plough); IFN--y (a gift from J. M. Mencia-Huerta, Institut Beaufour, Paris); TNF-a and anti-TNF-a mAb (Genzyme); human IgE (Stallergene, Paris), and goat anti-human IgE (Nordic, Tilburg, The Netherlands). Polymyxin B, LPS (Escherichia coli 055, L-2880), NG-monomethyl-L-arginine (L-NMMA), D-NMMA, L-arginine, D-arginine, superoxide dismutase (SOD), and catalase were all obtained from Sigma.Cells. Human mononuclear cells were obtained by Ficoll gradient separation of peripheral blood leukocytes from healthy volunteers. Monocytes were separated from lymphocytes by adherence to plastic dishes coated with fetal calf serum as described (24). After this procedure, >90% of cells expressed CD14 antigen and displayed cytochemical characteristics of monocytes (24). The cells were then incubated in Dulbecco's modified Eagle's medium (DMEM) supplemented with nonessential L-amino acids, sodium pyruvate, glutamine, penicillin, streptomycin, and 10% (vol/vol) fetal calf serum (all from GIBCO). The culture medium was routinely controlled for the absence of a direct activation effect on human monocytes (CD23 expression and TNF-a production as activation Abbreviations: mAb, monoclonal antibody; CD23 mAb, anti-CD23 mAb; IgE-IC, IgE-anti-IgE immune complexes; L-NMMA, NA3-monomethyl-L-arginine; LPS, lipopolysaccharide; NOS, NO synthase; iNOS, inducible NOS; IFN-y, interferon y; IL, interleukin; TNF-a, tumor necrosis factor ai; SOD, superoxide dismutase; HPRT, hypoxanthine phosphoribosyltransferase. tTo whom reprint requests should be ad...

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“…Cross-linking of surface CD23 promotes the generation of IL-1, IL-6, TNF-α, H 2 O 2 and nitric oxide synthase-2 (NOS2)-mediated NO through NFκB- and AP-1-dependent mechanisms [5], [6], [7], [8], [9]. We and others have also demonstrated the role of CD23 during inflammation in both Th1 and Th2 response [1], [7], [9].…”

Section: Introductionmentioning

confidence: 90%

Molecular Blocking of CD23 Supports Its Role in the Pathogenesis of Arthritis

Rambert¹,

Mamani-Matsuda²,

Moynet³

et al. 2009

PLoS ONE

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BackgroundCD23 is a differentiation/activation antigen expressed by a variety of hematopoietic and epithelial cells. It can also be detected in soluble forms in biological fluids. Initially known as the low-affinity receptor for immunoglobulin E (FcεRII), CD23 displays various other physiologic ligands such as CD21, CD11b/c, CD47-vitronectin, and mannose-containing proteins. CD23 mediates numerous immune responses by enhancing IgE-specific antigen presentation, regulating IgE synthesis, influencing cell differentiation and growth of both B- and T-cells. CD23-crosslinking promotes the secretion of pro-inflammatory mediators from human monocytes/macrophages, eosinophils and epithelial cells. Increased CD23 expression is found in patients during allergic reactions and rheumatoid arthritis while its physiopathologic role in these diseases remains to be clarified.Methodology/Principal FindingsWe previously generated heptapeptidic countrestructures of human CD23. Based on in vitro studies on healthy and arthritic patients' cells, we showed that CD23-specific peptide addition to human macrophages greatly diminished the transcription of genes encoding inflammatory cytokines. This was also confirmed by significant reduction of mediator levels in cell supernatants. We also show that CD23 peptide decreased IgE-mediated activation of both human and rat CD23+ macrophages. In vivo studies in rat model of arthritis showed that CD23-blocking peptide ameliorates clinical scores and prevent bone destruction in a dose dependent manner. Ex-vivo analysis of rat macrophages further confirmed the inhibitory effect of peptides on their activation. Taken together our results support the role of CD23 activation and subsequent inflammatory response in arthritis.ConclusionCD23-blocking peptide (p30A) prevents the activation of monocytes/macrophages without cell toxicity. Thus, targeting CD23 by antagonistic peptide decreases inflammatory markers and may have clinical value in the treatment of human arthritis and allergic reactions involving CD23.

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Involvement of cyclic AMP and nitric oxide in immunoglobulin E-dependent activation of Fc epsilon RII/CD23+ normal human keratinocytes.

Cited by 50 publications

References 23 publications

CD23 Mediates Antimycobacterial Activity of Human Macrophages

CD23 Mediates Antimycobacterial Activity of Human Macrophages

The killing of Leishmania major by human macrophages is mediated by nitric oxide induced after ligation of the Fc epsilon RII/CD23 surface antigen.

Molecular Blocking of CD23 Supports Its Role in the Pathogenesis of Arthritis

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