19S IgM Rheumatoid Factor-7S IgG Rheumatoid Factor Immune Complexes Isolated in Sera of Patients with Juvenile Rheumatoid Arthritis

Moore, Terry L.; Osborn, Thomas G.; Dorner, Robert W.

doi:10.1203/00006450-198610000-00017

Cited by 18 publications

(9 citation statements)

References 10 publications

(26 reference statements)

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“…Immune complex accumulation in circulation or tissues is implicated in a broad spectrum of human diseases characterized by acute and/or chronic inflammation, including rheumatoid arthritis [4,5], juvenile rheumatoid arthritis [6,7] and systemic lupus erythematosus [8,9]. Injury to host tissue in immune complex disease is attributed, in part, to the capacity of IgG‐containing complexes to activate the complement cascade, resulting in the release of phlogistic C4a and C3a peptides.…”

Section: Introductionmentioning

confidence: 99%

C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC

Xiao

Jarvis

2001

Clinical and Experimental Immunology

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Endothelial cells play a pivotal role in the initiation and perpetuation of inflammation. C1q, the first component of the classical pathway of complement, is a potent stimulus leading to endothelial cell activation and cytokine production. The specific cellular mechanisms through which endothelial cells are stimulated by C1q are not known. We stimulated human umbilical vein endothelial cells (HUVEC) with either monomeric C1q or C1q‐bearing immune complexes (C1q‐IC) in the presence or absence of inhibitors of protein tyrosine kinases (PTK) or mitogen‐activated protein kinases (MAPK). C1q‐IC, but not monomeric C1q, induced IL‐8 production in dose‐ and time‐dependent fashion. R3, a cross‐linking monoclonal IgM antibody against the126 kD phagocytic C1q receptor (C1qR), also stimulated IL‐8 production. IL‐8 mRNA accumulation was detected by Northern blot analysis within 2 h of stimulation by the immune complexes and was enhanced by the addition of cycloheximide. Secretion of IL‐8 by C1q‐IC stimulated HUVEC was completely blocked by the PTK inhibitor, genistein or the MAPK inhibitor, UO126. These experiments demonstrate that C1q‐IC‐induced production of IL‐8 in HUVEC is dependent upon the activation of PTK and MAPK. These findings also support a role for the phagocytic C1qR as an important activator of HUVEC by immune complexes.

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Section: Introductionmentioning

confidence: 99%

C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC

Xiao

Jarvis

2001

Clinical and Experimental Immunology

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“…Many previous studies have suggested that RF plays a central role in sustaining inflammatory events that lead to tissue damage (3,6), and some have demonstrated, by the hemolytic assay (2,5,6) and in IC studies (15), the complement-fixing ability of 19s IgM-RF in JRA. Separation and characterization studies, using multiple IC isolation methods, have detected 19s IgM-RF-IgG, hidden 19s IgM-RF-IgG, and 19s IgM-RF-7S IgG-RF containing IC in the sera of patients with JRA, in association with active clinical disease (15)(16)(17). Thus, the ability to demonstrate complementfixing 195 IgM-RF in the peripheral blood of a patient with JRA, either by the RF-PFC assay or IC detection methods, suggests a possible pathogenic role for 19s IgM-RF in JRA.…”

Section: Discussionmentioning

confidence: 99%

IgM rheumatoid factor plaque‐forming cells in juvenile rheumatoid arthritis

Moore

el-Najdawi

Dorner

1987

Arthritis & Rheumatism

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“…These complexes that were detected correlated with active disease. This study laid the groundwork for further defining individual constituents of the IC found in JIA patients ( 9 ).…”

Section: Early Studiesmentioning

confidence: 96%

Immune Complexes in Juvenile Idiopathic Arthritis

Moore

2016

Front. Immunol.

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Juvenile idiopathic arthritis (JIA) reflects a group of clinically heterogeneous, autoimmune disorders in children characterized by chronic arthritis and hallmarked by elevated levels of circulating immune complexes (CICs) and associated complement activation by-products in their sera. Immune complexes (ICs) have been detected in patients’ sera with JIA utilizing a variety of methods, including the anti-human IgM affinity column, C1q solid-phase assay, polyethylene glycol precipitation, Staphylococcal Protein A separation method, anti-C1q/C3 affinity columns, and FcγRIII affinity method. As many as 75% of JIA patients have had IC detected in their sera. The CIC proteome in JIA patients has been examined to elucidate disease-associated proteins that are expressed in active disease. Evaluation of these ICs has shown the presence of multiple peptide fragments by SDS-PAGE and 2-DE. Subsequently, all isotypes of rheumatoid factor (RF), isotypes of anti-cyclic citrullinated peptide (CCP) antibodies, IgG, C1q, C4, C3, and the membrane attack complex (MAC) were detected in these IC. Complement activation and levels of IC correlate with disease activity in JIA, indicating their role in the pathophysiology of the disease. This review will summarize the existing literature and discuss the role of possible protein modification that participates in the generation of the immune response. We will address the possible role of these events in the development of ectopic germinal centers that become the secondary site of plasma cell development in JIA. We will further address possible therapeutic modalities that could be instituted as a result of the information gathered by the presence of ICs in JIA.

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19S IgM Rheumatoid Factor-7S IgG Rheumatoid Factor Immune Complexes Isolated in Sera of Patients with Juvenile Rheumatoid Arthritis

Cited by 18 publications

References 10 publications

C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC

C1q-bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells (HUVEC) through protein tyrosine kinase- and mitogen-activated protein kinase-dependent mechanisms: evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC

IgM rheumatoid factor plaque‐forming cells in juvenile rheumatoid arthritis

Immune Complexes in Juvenile Idiopathic Arthritis

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