FcγR‐Dependent Regulation of the Biosynthesis of Complement C3 by Murine Macrophages: the Modulatory Effect of IL‐6

Bajtay, Zsuzsa; Falus, András; Erdei, Anna; Gergely, J.

doi:10.1111/j.1365-3083.1992.tb02850.x

Cited by 8 publications

(1 citation statement)

References 22 publications

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“…This result indicates that Abs initiate complement activition in allograft rejection. Abs can activate circulating complement components (33), but also can increase the secretion of complement components by macrophages at the site of inflammation (34,35).…”

Section: Discussionmentioning

confidence: 99%

Cytokines Regulate the Pattern of Rejection and Susceptibility to Cyclosporine Therapy in Different Mouse Recipient Strains After Cardiac Allografting

Wang

Hosiawa

Min

et al. 2003

The Journal of Immunology

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We determined the role of cytokines in regulating the pattern of rejection and recipient susceptibility to cyclosporine (CsA) in a mouse cardiac allograft model. Hearts from C3H mice transplanted into untreated BALB/c (Th2-dominant) and C57BL/6 (Th1-dominant) mice showed different patterns of rejection. C3H allografts in BALB/c mice showed typical acute vascular rejection (AVR) with strong intragraft deposition and high serum levels of anti-donor IgG with predominant IgG1, while C3H allografts in C57BL/6 mice showed typical acute cellular rejection (ACR) with massive intragraft infiltration of CD4+ and CD8+ lymphocytes and low serum levels of anti-donor IgG with predominant IgG2a. Elevated intragraft mRNA expression of IL-2, IFN-γ, and IL-12 mRNA was present in C57BL/6 recipients, whereas allografts in BALB/c mice displayed increased IL-4 and IL-10 mRNA levels. CsA therapy completely inhibited ACR and induced indefinite allograft survival in C57BL/6 recipients, while the same therapy failed to prevent AVR, and only marginally prolonged graft survival in BALB/c recipients. In contrast, rapamycin blocked AVR, achieving indefinite survival in BALB/c recipients, but was less effective at preventing ACR in C57BL/6 recipients. The disruption of the IL-12 or IFN-γ genes in C57BL/6 mice shifted ACR to AVR, and resulted in concomitant recipient resistance to CsA therapy. Conversely, disruption of IL-4 gene in BALB/c mice markedly attenuated AVR and significantly prolonged allograft survival. These data suggest that the distinct cytokine profiles expressed by different mouse strains play an essential role in regulating the pattern of rejection and outcome of CsA/rapamycin therapy.

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Section: Discussionmentioning

confidence: 99%

Cytokines Regulate the Pattern of Rejection and Susceptibility to Cyclosporine Therapy in Different Mouse Recipient Strains After Cardiac Allografting

Wang

Hosiawa

Min

et al. 2003

The Journal of Immunology

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Scientific memory from the early nineties; a common project with professors late János Gergely and Anna Erdei

Falus

Bajtay

2021

BIOLOGIA FUTURA

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Based on the findings of common project 29 years ago, the Scandinavian J. of Immunology accepted and published our paper entitled by “FcγR-Dependent Regulation of the Biosynthesis of Complement C3 by Murine Macrophages: the Modulatory Effect of IL-6” (Bajtay et al. in SJI 35:195–201, 1992). In this report we attempt to review the previous results and evaluate them with our current concepts on the interaction between the actors of adaptive and innate immunity. Let us first to summarize the basic results and consequences from the paper from 1992. Abstract from 1991–1992: The effect of murine IgG isotypes (myeloma proteins) on the gene expression and secretion of the third component of complement (C3) has been studied using the in monocytoid cell line P388D1 and oil-elicited mouse peritoneal macrophages. It is demonstrated that the binding of lgG2a and lgG2b but not IgGl and IgG3 isotypes augments the biosynthesis of C3 both in the presence and in the absence of the phorbol myristate acetate in the case of both cell types. The multifunctional cytokine inlerleukin-6 (IL-6) alone reveals no effect on the gene expression of C3, but facilitates the effectiveness of mouse IgG2a and IgG2b. Confirming the role of FcgRll, a strong up-regulation of gene expression and secretion of C3 was found when macrophages were co-cultured with the F(ab')2 fragment of the FcγRII-specific monoclonal antibody 2.4 G2.

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Heparin suppresses lipopolysaccharide-induced monocyte production of several cytokines, but simultaneously stimulates C3 production

Høgåsen¹,

Abrahamsen²

1995

Thrombosis Research

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FcγR‐Dependent Regulation of the Biosynthesis of Complement C3 by Murine Macrophages: the Modulatory Effect of IL‐6

Cited by 8 publications

References 22 publications

Cytokines Regulate the Pattern of Rejection and Susceptibility to Cyclosporine Therapy in Different Mouse Recipient Strains After Cardiac Allografting

Cytokines Regulate the Pattern of Rejection and Susceptibility to Cyclosporine Therapy in Different Mouse Recipient Strains After Cardiac Allografting

Scientific memory from the early nineties; a common project with professors late János Gergely and Anna Erdei

Heparin suppresses lipopolysaccharide-induced monocyte production of several cytokines, but simultaneously stimulates C3 production

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