Suppression of mitogen‐induced peripheral B cell differentiation by soluble Fcγ receptors released from lymphocytes

Lêthibichthuy,; Samarut, C; Brochier, J; Fridman, Wolf‐Herman; Revillard, Jean‐Pierre

doi:10.1002/eji.1830101116

Cited by 35 publications

(8 citation statements)

References 14 publications

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“…In regard to negative signals, T suppressor cells that preferentially inhibited IgA (4), IgE (5), and IgG2a and IgG2b (6) plaqueforming cells (pfc) were reported. Immunoglobulin-binding factor(s) [IBF(s)] that inhibit the differentiation of B cells to pfc have been described (7,8). Further studies of this factor by Fridman et al (9) demonstrated that IBF is the soluble form of Fcy receptor expressed on a T-cell subset.…”

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confidence: 99%

Isotype regulation of antibody production: T-cell hybrids can be selectively induced to produce IgG1 and IgG2 subclass-specific suppressive immunoglobulin-binding factors.

Löwy¹,

Brézin²,

Néauport–Sautès³

et al. 1983

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

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T2D4, a T-cell hybrid, spontaneously secretes suppressive immunoglobulin factor(s); when incubated with purified monoclonal mouse immunoglobulins, this hybrid produces high levels of immunoglobulin-binding factors specific for the subclass of the inducing immunoglobulin. Thus, we were able to induce the production of IgGI-or IgG2-specific inhibitory factors by the same T2D4 T-cell hybrid. These subclass-specific suppressive factors bind selectively to the IgGI or IgG2 subclasses and inhibit specifically the secretion of antibodies of the corresponding subclass. Our results favor a model of negative regulation of isotype expression in which a given isotype triggers suppressor mechanism(s) specifically inhibiting its production.It has been established that B cells are not precommitted for the secretion of a given isotype (1, 2). In some experiments, 106 spleen cells from DNP-Ova-immunized animals were used, and results were similar. pfc were measured on day 5. IBF-containing samples were added at various dilutions at the initiation of culture. In some instances the suppressor effects were also tested in a cooperative response between poly(Glu,Ala,Tyr)-primed lymph node cells and DNPprimed B cells as described (6).IgGI, IgG2a, IgG2b, and IgA pfc Assays. Hemolytic plaque assays were performed as described (6). IgGI 2323The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisenent" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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mentioning

confidence: 99%

Isotype regulation of antibody production: T-cell hybrids can be selectively induced to produce IgG1 and IgG2 subclass-specific suppressive immunoglobulin-binding factors.

Löwy¹,

Brézin²,

Néauport–Sautès³

et al. 1983

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

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“…FcyR on inflammatory cells in peripheral blood are involved in several important patho-physiologic phenomena: binding and phagocytosis of antibody-coated particles, antibody dependent cytotoxicity, the release of soluble mediators of inflammation such as prostaglandins and hydrolytic enzymes and suppression of mitogen-induced B lymphocyte differentiation and Ig production (15,27). Our studies indicate that FcyR are generally expressed on cells in inflamed tissue.…”

Section: Discussionmentioning

confidence: 64%

In situ demonstration of Fcγ‐receptors in human chronic marginal and periodontitis

Johannessen¹,

Nilsen²,

Matre

1987

J Oral Pathology Medicine

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The distribution of receptors for the Fc portion of IgG (FcγR) in chronic marginal and apical periodontitis were studied by using a monoclonal antibody against placental FcγR and soluble immune complexes as indicators. Cryostat sections were used in indirect immunofluorescence technique. FcγR were detected on varying numbers of cells in the inflammatorry cell infiltrates, on endothelial cells of certain vessels and in fibrous tissue. In chronic marginal periodontitis FcγR were also observed on cells within the oral gingival epithelium (OGE) and the pocket epithelium (PE). There was a distinct fluorescence in stratum spinosum and occasionally in stratum basale of OGE and in the coronal portion of the PE. FcγR on Langerhans cells could not be demonstrated. In apical periodontitis FcγR were also detected on cells within the epithelium. In some cases epithelium in periapical cysts was positive. Soluble immune complexes bound to morphologically similar, but fewer cells compared to the monoclonal antibody against FcγR. The results indicate that FcγR are generally expressed on cells in inflamed tissue. Thus, this presence of FcγR on certain specialized cells such as endothelial cells and keratinocytes, may endow these cells with functions previously thought to be restricted to cells of the lymphoreticular system.

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“…Several cell types may eontribute to the binding of EA and IgG immune complexes to gingival infiltrates, most likely B lymphocytes and monocytes/macrophages, although NK cells and possibly suppressor/ eytotoxic T cells may also eontribute. These receptors may be involved in several pathophysiologic phenomena: binding and phagocytosis of antibody-coated particles, antibody-dependent cytotoxicity, the release of soluble mediators of inflammation such as prostaglandins and hydrolytic enzymes and suppression of mitogen-induced B cell differentiation (Zuckerman & Douglas 1979, Le thi Bich-Thuy et al 1980.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms involved in the binding of IgG immune complexes to sections of inflamed gingiva

Kristoffersen

Johannessen

Tönder

et al. 1985

J of Periodontal Research

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The binding of paniculate (sensitized sheep erythrocytes = EA) and soluble (horse radish peroxidase (HRP)-anti-HRP) IgG immune complexes to cryostat sections of inflamed human gingiva was studied. EA bound preferentially to inflammatory cell infiltrates in all biopsy specimens, and HRP-anti-HRP complexes were found to bind to the surface of mononuclear cells. Binding of EA was abolished by treatment of cryostat sections with 1 mM periodic acid (30 min) or 4% formaldehyde (10 min). Binding was also abolished by exposure of sections to cold ethanol for 5 min. No binding of fluorescein labelled, heat aggregated human IgG to sections of washed and ethanol-fixed biopsies of inflamed human gingiva was observed. Results of inhibition experiments with rabbit and human native or heat aggregated IgG, rabbit and human IgG Fc and IgG F(ab)2fragments, human IgGl and IgG2, mildly reduced and alkylated human IgG and with rabbit anti-human Clq, indicated that the binding is not due to activated Cl or to the presence of rheumatoid factors. Our flndings are consistent with the concept that the binding is due to the presence of IgG Fc receptors (IgGFcR) on mononuclear cells. Ethanol fixation of specimens compromises any conclusions regarding igGFcR activity in the tissues.

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Suppression of mitogen‐induced peripheral B cell differentiation by soluble Fcγ receptors released from lymphocytes

Cited by 35 publications

References 14 publications

Isotype regulation of antibody production: T-cell hybrids can be selectively induced to produce IgG1 and IgG2 subclass-specific suppressive immunoglobulin-binding factors.

Isotype regulation of antibody production: T-cell hybrids can be selectively induced to produce IgG1 and IgG2 subclass-specific suppressive immunoglobulin-binding factors.

In situ demonstration of Fcγ‐receptors in human chronic marginal and periodontitis

Mechanisms involved in the binding of IgG immune complexes to sections of inflamed gingiva

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