Antigen‐antibody complexes suppress antibody production by mouse plasmacytoma cells <i>in vitro</i>

Abbas, Abul K.; Klaus, G. G. B.

doi:10.1002/eji.1830080315

Cited by 31 publications

(9 citation statements)

References 11 publications

(6 reference statements)

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“…This was supported by further experiments (Abbas & Klaus 1978) which showed that immune complexes containing DNPkeyhole limpet hemocyanin (KLH) (an antigen which had no effect per se), and mouse anti-DNP or anti-KLH antibodies also inhibited M315 antibody production. This was supported by further experiments (Abbas & Klaus 1978) which showed that immune complexes containing DNPkeyhole limpet hemocyanin (KLH) (an antigen which had no effect per se), and mouse anti-DNP or anti-KLH antibodies also inhibited M315 antibody production.…”

Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 89%

“…It appeared that with these cells, there was something unique about the presentation of the hapten on an Ig carrier. This was supported by further experiments (Abbas & Klaus 1978) which showed that immune complexes containing DNPkeyhole limpet hemocyanin (KLH) (an antigen which had no effect per se), and mouse anti-DNP or anti-KLH antibodies also inhibited M315 antibody production. Even complexes containing the M315 antibody itself were effective.…”

Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 89%

“…These observations strongly suggested that the inactivation was an active process, mediated initially by antigen-S-Ig interaction, and not simply due to passive mopping up of secreted antibody by cell-bound antigen (Klaus 1976a) In an attempt to investigate the mechanisms involved in greater detail, we subsequently studied the effects of antigen on a relatively homogeneous population of AFC, namely the anti-DNP antibody secreting plasmacytoma MOPC 315 , Abbas & Klaus 1978. These experiments showed that DNP-conjugates of gamma globulins (bovine, rabbit and human), but not of polysaccharides and other proteins, inhibited both the secretion and synthesis of M315 antibody in vitro.…”

Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 99%

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Irreversible Receptor Modulation on B Lymphocytes and the Control of Antibody‐Forming Cells by Antigen

Klaus¹

1979

Immunological Reviews

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Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 89%

Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 89%

Section: Inactivation Of Antibody-forming Cells By Antigen or Antigementioning

confidence: 99%

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Irreversible Receptor Modulation on B Lymphocytes and the Control of Antibody‐Forming Cells by Antigen

Klaus¹

1979

Immunological Reviews

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“…Some researchers have claimed that F(ab')2 fragments are not suppressive (Bruggemann and Rajewsky, 1982;Looney and Abraham, 1984;Nicholas and Sinclair, 1969) and others have claimed that they arc equally suppressive as intact IgG (Abbas and Klaus, 1978;Cerottini et al, 1969;Dai and Moller, 1988;Enriquez-Rincon and Klaus, 1984;Klaesson et al, 1996;Lees and Sinclair, 1973;Wason and Fitch, 1973). One of the most frequently used way of analyzing this is to compare the suppressive ability of intact IgG with that of F(ab')2 fragments (thai the Fc part has been enzymaticaltydigested).…”

Section: Introductionmentioning

confidence: 99%

Fc‐Dependent Monoclonal IgG1‐Mediated Suppression of Antibody Response

Kayhan

Aybay

2004

Immunological Investigations

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It has been known for a long time that passively administered antibodies (Abs) or immune complexes regulate the immune response to their specific antigen (Ag). IgG may sometimes suppress the humoral immune response against soluble antigens. The exact mechanism behind this phenomenon has not been understood yet and the requirement for the Fc part is still a matter of controversy. The present study was undertaken to clarify whether there is a true IgG-mediated Fc-dependent suppression of the immune response. Antigen and monoclonal antibody (mAb) used in this study were recombinant human interferon gamma (r-hIFN-gamma) and mouse monoclonal antibodies specific for human IFN-gamma [anti-hIFN-gamma mAb (CAy-IFNgamma38)] respectively. An intact IgG-free preparation of Fab plus various Fc fragments was prepared from papain-digested CAy-IFNgamma38. Ag/IgG and Ag/Fab complexes were prepared at various molar ratios. Keeping the Ag doses constant, mice were immunized either with Ag, Ag/IgG or Ag/Fab complexes. Primary immunization and the boosting were performed with the samples in complete and incomplete Freund's adjuvants respectively. Specific antibody levels were measured by an ELISA. Immunization performed with Ag/Fab complexes even at a molar ratio of 1:1.36 did not result in marked suppression of the response when compared to that of Ag only-immunization. In contrast, Ag/IgG complexes resulted in nearly 90% suppression of the antibody response. Our observations suggest that Fc part of IgG molecule plays a crucial role in suppression of the in vivo antibody response against the Ag when complexed with intact IgG.

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“…Thus early work with the murine plasmacytomas MOPC 3 15 and MOPC 460 showed that idiotypic specific tumour rejection can be elicited by immunizing with the myeloma proteins (Rohrer and Lynch, 1979). In addition, antigens in tolerogenic form (Abbas and Klaus, 1977), antigen antibody complexes (Abbas and Klaus, 1978), carrier specific helper and 0278-0232/88/02008346 $05.00 0 1988 by John Wiley & Sons, Ltd. suppressor T cells (Rohrer and Lynch, 1977), idiotypic specific T cells (Abbas et al, 1980) and alloreactive T cells (Abbas 1979), have all been shown to be capable of modulating myeloma cell growth and antibody secretion. Clinical studies likewise point to a role for host modifiers in tumours of B cell lineage.…”

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confidence: 99%

Biology of multiple myeloma—host‐tumour interactions and immune regulation of disease activity

1988

Hematological Oncology

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Multiple myeloma is a B lineage tumour, the neoplastic cells of which secrete a monoclonal idiotypic paraprotein and have a characteristic plasma B cell surface antigen expression, i.e. CIg+ , SIg-,PCA-I +,CD6+,CD19--,CD20-,HLA-DR-,CDlO-,Tdt-.Inaddition,anantigen shared with T blasts, i.e. TIO, CD38 is also present on plasma cells. Immunoglobulin gene rearrangements of both heavy and light chains are also seen (Foon rt al., 1982; Rosen et al., 1986).Both host-tumour and tumour-host interactions occur in myeloma and may reflect immunological regulatory mechanisms. For example there is considerable evidence to show that multiple myeloma produces a unique immunodeficiency state in the host quite unlike that produced by most cancers. Thus patients with myeloma (and mice-bearing pristane induced plasmacytomas) have hypogammaglobulinaemia, an impaired primary immune response to both T-dependent and T-independent antigens, but have a a relatively preserved secondary response and normal or near normal cell-mediated immunity (Ulrich and Zolla-Pazner, 1982; Joshua et al., 1979). This immunosuppressive effect occurs at relatively low tumour loads and is believed to be a specific effect of the malignancy. The exact aetiology of this effect is unknown, but it is postulated to be due to lack of normal B cells, active immunoregulatory circuits and defects in macrophage handling of antigen. Macrophage abnormalities could either take the form of sequestrian of antigen and/or inadequate antigen presentation. For example, mice bearing the plasmacytoma TEPCl83 have an absolute increase in macrophages in the red pulp of the spleen without any change in splenic marginal zone macrophages providing a mechanism for antigen sequestration in non-antigen presenting cells. A parallel is seen in the splenic histology of experimental murine malaria where suppression of primary and secondary antibody responses similar to that seen in the murine plasmacytomas has been reported (Joshua et al., 1980). Alternatively, on the basis of in vitro data, macrophages may act as suppressor cells. These suppressor macrophages are believed to be induced by a factor secreted by plasmacytoma cells and they in turn release a second humoral substance termed 'plasmacytoma-induced macrophage substance' (PIMS), which inhibits B cell proliferation and antibody production (Katzmann, 1978).In addition to the effect the tumour has on the host's immune system, there is suggestive evidence from the murine plasmacytoma model that the host's immunological mechanisms can modulate tumour growth. Thus early work with the murine plasmacytomas MOPC 3 15 and MOPC 460 showed that idiotypic specific tumour rejection can be elicited by immunizing with the myeloma proteins (Rohrer and Lynch, 1979). In addition, antigens in tolerogenic form (Abbas and Klaus, 1977), antigen antibody complexes (Abbas and Klaus, 1978), carrier specific helper and

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Antigen‐antibody complexes suppress antibody production by mouse plasmacytoma cells in vitro

Cited by 31 publications

References 11 publications

Irreversible Receptor Modulation on B Lymphocytes and the Control of Antibody‐Forming Cells by Antigen

Irreversible Receptor Modulation on B Lymphocytes and the Control of Antibody‐Forming Cells by Antigen

Fc‐Dependent Monoclonal IgG1‐Mediated Suppression of Antibody Response

Biology of multiple myeloma—host‐tumour interactions and immune regulation of disease activity

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