Effects of Anti-C4 Antibody on Complement Production by Splenic and Peritoneal Macrophages

Goldman, John N.; O'Rourke, K S; McMannis, John D.; Goldman, Margaret B.

doi:10.1159/000463027

Cited by 3 publications

(3 citation statements)

References 9 publications

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“…Antibody treatment induced specific suppression of C4 in peritoneal cell monolayers. Further studies revealed that long-term C4 suppression is actively maintained by a soluble suppressor factor (FsC4) (67)(68)(69)(70). Most of those experiments were carried out in vitro cellular models from guinea pig.…”

Section: Diversity Of Complement C4 Genes and Proteinsmentioning

confidence: 99%

Complement C4, Infections, and Autoimmune Diseases

Wang

Liu

2021

Front. Immunol.

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Complement C4, a key molecule in the complement system that is one of chief constituents of innate immunity for immediate recognition and elimination of invading microbes, plays an essential role for the functions of both classical (CP) and lectin (LP) complement pathways. Complement C4 is the most polymorphic protein in complement system. A plethora of research data demonstrated that individuals with C4 deficiency are prone to microbial infections and autoimmune disorders. In this review, we will discuss the diversity of complement C4 proteins and its genetic structures. In addition, the current development of the regulation of complement C4 activation and its activation derivatives will be reviewed. Moreover, the review will provide the updates on the molecule interactions of complement C4 under the circumstances of bacterial and viral infections, as well as autoimmune diseases. Lastly, more evidence will be presented to support the paradigm that links microbial infections and autoimmune disorders under the condition of the deficiency of complement C4. We provide such an updated overview that would shed light on current research of complement C4. The newly identified targets of molecular interaction will not only lead to novel hypotheses on the study of complement C4 but also assist to propose new strategies for targeting microbial infections, as well as autoimmune disorders.

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Section: Diversity Of Complement C4 Genes and Proteinsmentioning

confidence: 99%

Complement C4, Infections, and Autoimmune Diseases

Wang

Liu

2021

Front. Immunol.

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“…Long-term treatment of infected IC-21 cells with anti-MV antibody induces suppression of MV protein synthesis that continues for days after treatment is terminated. Having demonstrated that a 2-h exposure to anti-MV serum suppressed viral protein synthesis in infected cells, we next determined whether extended treatment periods prolonged the suppression in a manner that was similar to what had been observed for intrinsic cell products (15)(16)(17)(18)(19)(20)(21)(22)(23)(24). In the experiment whose results are shown in Fig.…”

Section: Short-term Treatment Of Infected Ic-21 Cells With Anti-mv Anmentioning

confidence: 73%

“…H, M, and F proteins are proteins that complex with the viral enve- Our results from experiments on the immune regulation of viral proteins are consistent with our results from experiments on the immune regulation of proteins normally expressed by macrophages, e.g., complement components. For several years our laboratory has been studying the mechanisms whereby synthesis of individual complement components can be suppressed by in vivo or in vitro treatment of primary macrophages or hepatocytes with specific antibody or hyperimmune lymphoid cells directed against that component (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)32). Experiments with in vivo and in vitro complement suppression have demonstrated the following characteristics and requirements for antigenic suppression.…”

Section: Discussionmentioning

confidence: 99%

Suppression of measles virus expression by noncytolytic antibody in an immortalized macrophage cell line

Goldman

O'Bryan

Buckthal

et al. 1995

J Virol

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Immune regulation of measles virus (MV) expression was studied in a persistently infected mouse macrophage cell line. Synthesis of both membrane-associated and internal MV antigens was suppressed when infected macrophages were treated with polyclonal rabbit anti-MV antibody that was specific for MV proteins. Persistently infected macrophages were treated for 3, 5, or 7 days with increasing doses of anti-MV antibody. All MV proteins were down-regulated 2 days after treatment was terminated. One week after treatment was terminated, down-regulation was still evident but to a lesser degree. MV protein synthesis was suppressed whether or not complement components were inactivated by heating all serum supplements and antibodies. However, when complement was active, cell lysis accounted for some of the reduced MV protein synthesis. When lytic destruction of infected cells by antibody and complement was prevented by inactivation of complement, antibody alone reduced the cellular synthesis of viral proteins by noncytolytic mechanisms. The absence of cell death in the absence of complement was confirmed by the lack of 51Cr release from labeled cells, the lack of reduction in cell number, and the lack of a decrease in total protein synthesis when radiolabeled infected cells were treated with antibody. It is noteworthy that low doses of antibody were optimal for suppression in the longer-term experiments and did not cause lysis, even in the presence of active complement. Since infected macrophages disseminate virus in measles infection, noncytolytic regulation of these cells by antibody may supplement viral clearance by cytolytic T cells and other immune mechanisms.

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T lymphocytes mediate immunologic control of C3 gene expression

1992

Self Cite

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Immunologic control of C3 gene expression by tissue macrophages can be accomplished by treatment of spleen fragments with anti-C3 antibody. We now demonstrate that suppression of C3 requires participation of T lymphocytes of both the CD4+ and CD8+ phenotypes. Pretreatment of splenic tissue with anti-Thy-1.2 monoclonal antibody blocks the ability of the anti-C3 antibody to induce C3 suppression. Reduction in either the CD4+ or CD8+ subpopulations of T lymphocytes also abrogates C3 suppression demonstrating that both T cell subsets are required in addition to the inducing antibody. Artificially elevating intracellular levels of cAMP with cholera toxin can partially substitute for the effects mediated by T cells in this reaction. Therefore, normal expression of the C3 gene can be suppressed by a regulatory network that requires the presence of a specific inducing antibody and T lymphocytes of both the CD4+ and CD8+ subsets. This regulatory network has many similarities to regulatory networks that have been well documented in suppression of specific murine immunoglobulin allotypes.

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Effects of Anti-C4 Antibody on Complement Production by Splenic and Peritoneal Macrophages

Cited by 3 publications

References 9 publications

Complement C4, Infections, and Autoimmune Diseases

Complement C4, Infections, and Autoimmune Diseases

Suppression of measles virus expression by noncytolytic antibody in an immortalized macrophage cell line

T lymphocytes mediate immunologic control of C3 gene expression

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