T lymphocytes mediate immunologic control of C3 gene expression

Goldman, Margaret B.; Knovich, Mary Ann; Goldman, John N.

doi:10.1002/eji.1830221212

Cited by 2 publications

(2 citation statements)

References 26 publications

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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%

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

confidence: 73%

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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Immunohistochemistry of Complement Response on Human Renal Cell Carcinoma Biopsies

Magyarlaki

Mosolits

Baranyay

et al. 1996

Tumori

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The goal of the study was to characterize the complement humoral and cellular antitumor responses on primary renal cell carcinoma biopsies. As an original observation, complement activation was found on 11/22 cases. Classical complement pathway activation was characterized by tumor C1q complement protein and IgG deposition (5/22 cases). Alternative or nonimmune complement pathway activation was seen as tissue deposition of C3 (6/22 cases). The membrane attack complex was present in cases with alternative complement pathway activation at the sites of tumor necrosis. Renal cell carcinomas with complement activation overexpressed at least one of the complement regulatory factors (membrane cofactor protein, decay accelerating factor, membrane attack complex inhibitor) and major histocompatibility complex class II molecules. Tumor infiltrating lymphocytes were present in most of the renal cell carcinomas with complement activation (8/11). However, the number of tumor-infiltrating lymphocytes was correlated with the intensity of major histo-compatibility complex-II expression in 18/22 cases. Detection of complement activation and immune cell infiltrates on renal cell carcinoma primary biopsies may serve as a new predictive factor for immunotherapy.

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T lymphocytes mediate immunologic control of C3 gene expression

Cited by 2 publications

References 26 publications

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

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

Immunohistochemistry of Complement Response on Human Renal Cell Carcinoma Biopsies

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