In vitro studies on the Fc-receptor function of mononuclear phagocytes in rheumatoid arthritis: Relation between the Fc-receptor blockade and the concanavalin A-binding capacity of autologous immunoglobulin G

1986 ◽  
Vol 6 (6) ◽  
pp. 442-456 ◽  
Author(s):  
Michel G. Malaise ◽  
Paul Franchimont ◽  
Camille Houssier ◽  
Jean Closset ◽  
Georges Hennen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Concanavalin A ◽  
Immunoglobulin G ◽  
Binding Capacity ◽  
Fc Receptor ◽  
Mononuclear Phagocytes ◽  
In Vitro Studies ◽  
Receptor Blockade ◽  
Receptor Function

scholarly journals Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.

1979 ◽  
Vol 150 (3) ◽  
pp. 653-675 ◽  
Author(s):  
J A Griffin ◽  
F M Griffin
Keyword(s):  
T Lymphocytes ◽  
Complex Disease ◽  
Peritoneal Macrophages ◽  
Fc Receptor ◽  
Microbial Pathogens ◽  
Complement Receptor ◽  
Complement Receptors ◽  
Cellular Interactions ◽  
Receptor Function

The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.

scholarly journals Treatment of the anemia of rheumatoid arthritis with recombinant human erythropoietin: Clinical and in vitro studies

1989 ◽  
Vol 32 (5) ◽  
pp. 638-642 ◽  
Author(s):  
Robert T. Means ◽  
Nancy J. Olsen ◽  
Sanford B. Krantz ◽  
Emmanuel N. Dessypris ◽  
Stanley E. Graber ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Recombinant Human Erythropoietin ◽  
In Vitro Studies ◽  
Human Erythropoietin

scholarly journals Quercetin loaded nanoemulsion-based gel for rheumatoid arthritis: In vivo and in vitro studies

2019 ◽  
Vol 112 ◽  
pp. 108622 ◽  
Author(s):  
Jayanti P. Gokhale ◽  
Hitendra S. Mahajan ◽  
Sanjay J. Surana
Keyword(s):  
Rheumatoid Arthritis ◽  
In Vitro Studies

scholarly journals In vitro differentiation of human monocytes. Differences in monocyte phenotypes induced by cultivation on glass or on collagen.

1982 ◽  
Vol 156 (4) ◽  
pp. 1101-1114 ◽  
Author(s):  
G Kaplan ◽  
G Gaudernack
Keyword(s):  
Human Peripheral Blood ◽  
Surface Antigens ◽  
Fc Receptor ◽  
Mononuclear Phagocytes ◽  
Receptor Expression ◽  
Blood Monocytes ◽  
In Vitro Differentiation ◽  
Phagocytic Cells ◽  
Stage Of Development

We demonstrated that the in vitro differentiation of human peripheral blood monocytes to macrophages is dependent on the environment and conditions of monocyte culture. Cultivation of monocytes on glass or microexudate-coated glass gave rise to cells resembling foreign body granuloma macrophages. After an initial rise in Fc receptor- and C3 receptor-mediated phagocytosis, a progressive loss of Fc receptor expression and C3-mediated ingestion were observed. The monocyte surface antigens recognized by the anti-human monocyte monoclonal antibodies 1D5 and 63D3 were lost from the surface of the majority of cells cultured on glass and microexudates. A subpopulation of Fc receptor-positive cells that were 1D5 and 63D3 positive was retained in fully differentiated cell populations. In comparison, monocytes cultivated on collagen matrices gave rise to highly phagocytic cells resembling human resident tissue macrophages. Both Fc- and C3-mediated phagocytosis were enhanced and remained so during the entire length of culture. The surface antigens recognized by the 1D5 antibody, expressed on all freshly seeded monocytes, was maintained on the macrophages. The antigen recognized by the 63D3 antibody was not expressed on mature cells. The present evidence would indicate that variations in expression of phagocytic receptors and the surface antigens 1D5 and 63D3 can be ascribed to the stage of development of the macrophage or its stage of activation, rather than to independent subsets of mononuclear phagocytes.

Functional in vitro studies of recombinant human immunoglobulin G and immunoglobulin A anti-D

Transfusion ◽  
2007 ◽  
Vol 47 (2) ◽  
pp. 306-315 ◽  
Author(s):  
Leif Kofoed Nielsen ◽  
Trine Hefsgaard Green ◽  
Lars Norderhaug ◽  
Inger Sandlie ◽  
Morten Hanefeld Dziegiel
Keyword(s):  
Immunoglobulin G ◽  
Immunoglobulin A ◽  
In Vitro Studies ◽  
Human Immunoglobulin ◽  
Human Immunoglobulin G

scholarly journals POS0367 NLRC4 AND FC-γ-R CROSSTALK ON CD1C+ DENDRITIC CELLS DIFFERENTIALLY CONTRIBUTES TO RHEUMATOID ARTHRITIS IMMUNOPATHOLOGY

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 413.2-413
Author(s):  
C. Delgado-Arévalo ◽  
M. Calvet-Mirabent ◽  
A. Triguero-Martinez ◽  
E. Vazquez de Luis ◽  
A. Benguría-Filippini ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Dendritic Cells ◽  
Synovial Fluid ◽  
Cd4 T Cells ◽  
Treatment Initiation ◽  
Fc Receptor ◽  
Response To Therapy ◽  
Caspase 1

Background:Rheumatoid arthritis (RA) is an autoimmune disorder in which Th17 cells, B cells and inflammatory cytokines (1-3) contribute to joint tissue damage, however the role of specific myeloid populations to immunopathogenesis of RA remains unclear.Objectives:To address this question, we studied transcriptional, phenotypical and functional characteristics of monocytes (Mo), CD1c+ and CD141+ conventional dendritic cells (cDC) from RA patients.Methods:Frequencies and maturation patterns of Lin-CD14-HLADR+ plasmacytoid (CD11c-), CD1c+ and CD141+ cDC (CD11c+) subsets and CD14+ Mo from n=25 RA patients at baseline were analyzed by multicolor flow cytometry. In addition, longitudinal studies on the evolution of these populations after treatment initiation were conducted on a smaller group of RA patients. Moreover, CD1c+ and CD141+ cDC subsets and total Mo were sorted from the peripheral blood from n=4 untreated RA and healthy individuals and the synovial fluid from n=3 RA and chondrocalcinosis patients. Differential transcriptional patterns within each population were analyzed by RNAseq. Functional validation of targets were performed in vitro with cDC subsets isolated form the synoviual fluid of RA patients. Finally, silencing of expression of NLRC4 and NLRP3 on CD1c+cDCs was performed with specific siRNAs.Results:Both CD1c+ (p=0.0001) and CD141+ (p=0.0008) cDCs were significantly depleted from the blood and enriched in the synovial fluid from untreated RA patients, but proportions of CD1c+ cDCs were more significantly recovered after treatment initiation and associated with improved clinical parameters. In addition, specific increased expression levels of the IgG-Fc receptor CD64 on CD1c+ cDC was associated with higher DAS28 (p=0.0002). Moreover, differential transcriptional patterns of circulating CD1c+cDCs from RA patients were characterized by genes linked to toll-like receptor, Fc-receptor, inflammasome pathways and elevated CCR2 expression (p=0.016), while CD141+cDCs transcribed interferon-related genes. Importantly, CCR2+ CD64Hi CD1c+cDCs from the synovial fluid from RA patients transcribed proinflammatory cytokines such as IL1-β, CCL3 and IL-8, actively expressed the inflammasome mediator caspase 1 and were more effective activating pathogenic IFNγ+IL-17+ CD4+ T cells in vitro than CD141+ cDC (p=0.0019). These functional profiles could be artificially induced stimulating CD1c+ cDCs with dsDNA in the presence of IgGs and was dependent on caspase 1 and the NLRC4 inflammasome.Conclusion:Our data provides novel insights about specific activation and functional patterns on CD1c+cDC contributing to RA pathogenesis and identifies new sensors that could represent novel therapeutic target to treat RA.References:[1]Alvandpur N, Tabatabaei R, Tahamoli-Roudsari A, Basiri Z, Behzad M, Rezaeepoor M, et al. Circulating IFN-gamma producing CD4+ T cells and IL-17A producing CD4+ T cells, HLA-shared epitope and ACPA may characterize the clinical response to therapy in rheumatoid arthritis patients. Human immunology. 2020.[2]Nistala K, Adams S, Cambrook H, Ursu S, Olivito B, de Jager W, et al. Th17 plasticity in human autoimmune arthritis is driven by the inflammatory environment. Proceedings of the National Academy of Sciences of the United States of America. 2010;107(33):14751-6.[3]Chapuy-Regaud S, Nogueira L, Clavel C, Sebbag M, Vincent C, Serre G. IgG subclass distribution of the rheumatoid arthritis-specific autoantibodies to citrullinated fibrin. Clinical and experimental immunology. 2005;139(3):542-50.Disclosure of Interests:None declared

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