Suppression of in vitro antibody synthesis by immunoglobulin-binding factor.

Gisler, Roland H.; Fridman, Wolf‐Herman

doi:10.1084/jem.142.2.507

Cited by 119 publications

(32 citation statements)

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“…Fab fraction-mediated efficiency of pooled human IgG might be explained by anti-idiotypic activity against autoantibodies [11][12][13][14][15][16], by modulation of B and T lymphocyte functions through binding to these cells [16][17][18][19][20][21], by recognition and elimination of infectious agents associated with autoimmune diseases [10,22], or by modulation of the activity of various lymphokines, including IL-1, IL-6 and tumour necrosis factor (TNF) [23][24][25][26]. Through their Fc region, IgG could, among other possible mechanisms [7], increase the catabolism of autoantibodies [10], or decrease antibody production, via the production of soluble Fc receptors [27][28][29][30][31]. However, one of the most probable mechanisms that could explain the therapeutic activity of IgG pools is a temporary blockage of Fc receptors on phagocytic cells.…”

Section: Introductionmentioning

confidence: 99%

The mode of action of treatment by IgG of haemolytic anaemia induced by an anti-erythrocyte monoclonal antibody

Pottier

Pierard

Barclay

et al. 1996

Clinical and Experimental Immunology

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SUMMARYIn order to gain insight into the mechanisms by which the infusion of IgG can improve some autoimmune diseases, we induced haemolytic anaemia in mice by the injection of anti-erythrocyte MoAbs derived from NZB mice by S. Izui (Geneva). The IgG1 antibody 31-9D induces anaemia by erythrocyte sequestration in the spleen and liver, whereas the IgG2a antibody 34-3C triggers erythrophagocytosis (Shibata et al., Int Immunol 1990; 2:1133). Treatment of mice with pools of either human or mouse IgG clearly attenuated the anaemia induced by 34-3C, but not by 31-9D. Similar protection was obtained with human monoclonal IgGs from myeloma patients. Prior absorption by mouse erythrocytes did not affect the efficacy of the injected IgG. Treatment with Fc fragments also reduced the anaemia. In vitro experiments confirmed that 34-3C, but not 31-9D, triggered erythrocyte phagocytosis by murine macrophages. This process was completely inhibited by addition of polyclonal or myeloma IgG or of human Fc fragments. These results indicate that, in this model of autoimmune pathology, the protective effect of IgG is mediated by its interaction with the macrophage Fc receptors.

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Section: Introductionmentioning

confidence: 99%

The mode of action of treatment by IgG of haemolytic anaemia induced by an anti-erythrocyte monoclonal antibody

Pottier

Pierard

Barclay

et al. 1996

Clinical and Experimental Immunology

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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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“…Considerable evidence has been recently accumulated indicating that FcR ÷ cells participate significantly in regulating isotypespecific antibody responses. Suppressor T cells and their released soluble products, some of which are immunoglobulin-binding factors (IBF), that selectively inhibit synthesis of IgG~, IgG~a, and IgG2b have been demonstrated by other investigators (38,39). Similarly, in the IgA system FcRo~ + T cells generated in high quantities in IgA myeloma-bearing mice, have been shown to regulate the synthesis of IgA (40).…”

Section: Discussionmentioning

confidence: 98%

IgE class-restricted tolerance induced by neonatal administration of soluble or cell-bound IgE. Cellular mechanisms.

Chen¹,

Liu²,

Katz³

1984

The Journal of Experimental Medicine

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Unraveling the pathophysioiogy of IgE-mediated allergic disorders requires a thorough understanding of the complex mechanisms that control IgE antibody synthesis. The selective activation and further maturation of the IgE B cell are regulated by both antigen-specific and non-antigen-specific, but isotype-restricted, T cells and the soluble factors that they produce (1-6). Although the manner by which antigen-specific and isotype-restricted regulatory events are coordinated is still unresolved, studies of Ishizaka and colleagues (7-13) and of our group (14-19) indicate that the Fc determinants of IgE and the correspondingly specific Fc receptors for IgE (FcR~) ~ on lymphocytes contribute significantly to such regulatory mechanisms.IgE antibody responses can be significantly enhanced in experimental animals in which sensitization with antigen has been properly correlated with nonspecific perturbations such as low dose irradiation or treatment with immunosuppressive drugs (13,(20)(21)(22)(23). Similar perturbations, perhaps resulting from common respiratory virus infections (15), could be responsible for development of high IgE responses in individuals exposed to allergens over a sustained period of time (21), and are probably involved in the enhanced IgE production that accompanies parasite infections (22). Certain of the experimentally induced perturbations in normal mechanisms controlling IgE antibody responses can be selectively reversed by in vivo administration of biologically active soluble factors, obtained from body fluids of living animals (23). This is publication number 34 from the

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Suppression of in vitro antibody synthesis by immunoglobulin-binding factor.

Cited by 119 publications

References 19 publications

The mode of action of treatment by IgG of haemolytic anaemia induced by an anti-erythrocyte monoclonal antibody

The mode of action of treatment by IgG of haemolytic anaemia induced by an anti-erythrocyte monoclonal antibody

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

IgE class-restricted tolerance induced by neonatal administration of soluble or cell-bound IgE. Cellular mechanisms.

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