REGULATION OF THE IMMUNE RESPONSE BY IgM ANTIBODY: A PARADOXICAL SUPPRESSION OF THE <i>IN VITRO</i>
 PRIMARY IMMUNE RESPONSE TO SHEEP ERYTHROCYTES BY PASSIVE IgM.

Schrader, John W.

doi:10.1038/icb.1973.32

Cited by 11 publications

(3 citation statements)

References 4 publications

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“…This has been revealing with respect to IgM positive feedback. Schrader (1972) in our laboratory has shown that IgM preparations which give good augmentation in vivo of the antibody response to SRC are entirely ineffective in vitro. This was equally true whether whole spleen or T-depleted or macrophage-depleted cell populations were cultured.…”

Section: Antibody-mediated Tolerance In Vitromentioning

confidence: 99%

“…Such ATC-TDL contain less than 0.3 per cent B cells but collaborate more efficiently than do the ATC from the spl^ns of such mice (Feldmann & Sprent, unpublished). Thus the possibility that the IgM component of collaboration was made by contaminating B cells, unlikely since IgM antibody does not replace T cells (Schrader 1972), has been ruled out.…”

Section: D) Nature Of the Specific Collaborative Factor Made By T Helmentioning

confidence: 99%

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Tolerance, Enhancement and the Regulation of Interactions Between T Cells, B Cells and Macrophages

Feldmann

Nossal

1972

Immunological Reviews

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Section: Antibody-mediated Tolerance In Vitromentioning

confidence: 99%

Section: D) Nature Of the Specific Collaborative Factor Made By T Helmentioning

confidence: 99%

Tolerance, Enhancement and the Regulation of Interactions Between T Cells, B Cells and Macrophages

Feldmann

Nossal

1972

Immunological Reviews

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“…However. if the IgM is given 2 h after the antigen or if the stimulation is done in vitro, IgM may have a suppressive effeet on the antibody response [32,36]. These findings and the demonstration of increased splenic localization of SRBC after IgM inoculation [6] suggest that one mechanism of potentiation is the redistribution of antigen in a favourable manner for stimulation of antibody responses.…”

mentioning

confidence: 99%

Specific IgM Enhances and IgG Inhibits the Induction of Immunological Memory in Mice

Heyman

Wigzell

1985

Scand J Immunol

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The effect of priming mice with IgM anti-SRBC (sheep erythrocytes) together with SRBC or IgG anti-SRBC together with SRBC on the development and expression of memory cells was studied. Mice primed with specific IgM and SRBC showed a much more efficient secondary plaque-forming cell and serum antibody response after challenge with SRBC in an adoptive transfer system than did controls primed with SRBC only. The expression of this enhanced memory of IgM-primed spleen cells was counteracted by the high levels of internal IgG anti-SRBC (also the result of priming with IgM) when the mice, instead of being tested in adoptive transfers, were challenged directly. The antigen-specific feedback suppression of the primary antibody response by specific IgG antibodies was also seen to inhibit partially the development of memory cells. The suppressive effect on priming could be demonstrated both in adoptive transfer systems and after direct boost of the same mice that received the primary immunization. Both the IgM enhancement and the IgG suppression of memory cell development were antigen-specific, since no effect on the antibody response to a non-cross-reacting antigen, horse erythrocytes, was seen. The effect of these up- or down-regulations of immunological memory could be demonstrated after secondary injections as long as 90-280 days after priming.

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Specific IgM and Regulation of Antibody Responses

Sörman

Heyman

2017

Current Topics in Microbiology and Immunology

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Specific IgM, administered together with the antigen it recognizes, enhances primary antibody responses, formation of germinal centers, and priming for secondary antibody responses. The response to all epitopes on the antigen to which IgM binds is usually enhanced. IgM preferentially enhances responses to large antigens such as erythrocytes, malaria parasites, and keyhole limpet hemocyanine. In order for an effect to be seen, antigens must be administered in suboptimal concentrations and in close temporal relationship to the IgM. Enhancement is dependent on the ability of IgM to activate complement, but the lytic pathway is not required. Enhancement does not take place in mice lacking complement receptors 1 and 2 (CR1/2) suggesting that the role of IgM is to generate C3 split products, i.e., the ligands for CR1/2. In mice, these receptors are expressed on follicular dendritic cells (FDCs) and B cells. Optimal IgM-mediated enhancement requires that both cell types express CR1/2, but intermediate enhancement is seen when only FDCs express the receptors and low enhancement when only B cells express them. These observations imply that IgM-mediated enhancement works through several, non-mutually exclusive, pathways. Marginal zone B cells can transport IgM-antigen-complement complexes, bound to CR1/2, from the marginal zone and deposit them onto FDCs. In addition, co-crosslinking of the BCR and the CR2/CD19/CD81 co-receptor complex may enhance signaling to specific B cells, a mechanism likely to be involved in induction of early extrafollicular antibody responses.

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REGULATION OF THE IMMUNE RESPONSE BY IgM ANTIBODY: A PARADOXICAL SUPPRESSION OF THE IN VITRO PRIMARY IMMUNE RESPONSE TO SHEEP ERYTHROCYTES BY PASSIVE IgM.

Cited by 11 publications

References 4 publications

Tolerance, Enhancement and the Regulation of Interactions Between T Cells, B Cells and Macrophages

Tolerance, Enhancement and the Regulation of Interactions Between T Cells, B Cells and Macrophages

Specific IgM Enhances and IgG Inhibits the Induction of Immunological Memory in Mice

Specific IgM and Regulation of Antibody Responses

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