scholarly journals Neutrophils from the synovial fluid of patients with rheumatoid arthritis express the high affinity immunoglobulin G receptor, Fc γ RI (CD64): role of immune complexes and cytokines in induction of receptor expression

Immunology ◽  
1997 ◽  
Vol 91 (2) ◽  
pp. 266-273 ◽  
Author(s):  
J. A QUAYLE ◽  
F. WATSON ◽  
R. C. BUCKNALL ◽  
S. W. EDWARDS
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Immunoglobulin G ◽  
Immune Complexes ◽  
Receptor Expression ◽  
High Affinity ◽  
Immunoglobulin G Receptor

scholarly journals Number of individual ACPA reactivities in synovial fluid immune complexes, but not serum anti-CCP2 levels, associate with inflammation and joint destruction in rheumatoid arthritis

2018 ◽  
Vol 77 (9) ◽  
pp. 1345-1353 ◽  
Author(s):  
Azita Sohrabian ◽  
Linda Mathsson-Alm ◽  
Monika Hansson ◽  
Ann Knight ◽  
Jörgen Lysholm ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Immune Complexes ◽  
Magnetic Beads ◽  
Joint Destruction ◽  
Joint Pathology ◽  
A New Technique ◽  
Laboratory Measures

IntroductionIndividual patients with rheumatoid arthritis (RA) show divergent specific anti-citrullinated protein/peptide antibodies (ACPA) patterns, but hitherto no individual ACPA specificity has consistently been linked to RA pathogenesis. ACPA are also implicated in immune complexes (IC)-associated joint pathology, but until now, there has been no method to investigate the role of individual ACPA in RA IC formation and IC-associated pathogenesis.MethodsWe have developed a new technique based on IC binding to C1q-coated magnetic beads to purify and solubilise circulating IC in sera and synovial fluids (SF) from 77 patients with RA. This was combined with measurement of 19 individual ACPA in serum, SF and in the IC fractions from serum and SF. We investigated whether occurrence of individual ACPA as well as number of ACPA in these compartments was related to clinical and laboratory measures of disease activity and inflammation.ResultsThe majority of individual ACPA reactivities were enriched in SF as compared with in serum, and levels of ACPA in IC were regulated independently of levels in serum and SF. No individual ACPA reactivity in any compartment showed a dominating association to clinical and laboratory measures of disease activity and severity. Instead, the number of individual ACPA reactivities in the IC fraction from SF associated with a number of markers of joint destruction and inflammation.ConclusionsOur data highlight the polyclonality of ACPA in joint IC and the possibility that a broad ACPA repertoire in synovial fluid IC might drive the local inflammatory and matrix-degrading processes in joints, in analogy with antibody-induced rodent arthritis models.

scholarly journals Prostacyclin-IP signaling and prostaglandin E2-EP2/EP4 signaling both mediate joint inflammation in mouse collagen-induced arthritis

2006 ◽  
Vol 203 (2) ◽  
pp. 325-335 ◽  
Author(s):  
Tetsuya Honda ◽  
Eri Segi-Nishida ◽  
Yoshiki Miyachi ◽  
Shuh Narumiya
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Joint Inflammation ◽  
Synovial Fibroblasts ◽  
The Other ◽  
Receptor Subtype ◽  
Significant Suppression ◽  
Wild Type ◽  
Collagen Induced Arthritis

Prostaglandin (PG)I2 (prostacyclin [PGI]) and PGE2 are abundantly present in the synovial fluid of rheumatoid arthritis (RA) patients. Although the role of PGE2 in RA has been well studied, how much PGI2 contributes to RA is little known. To examine this issue, we backcrossed mice lacking the PGI receptor (IP) to the DBA/1J strain and subjected them to collagen-induced arthritis (CIA). IP-deficient (IP−/−) mice exhibited significant reduction in arthritic scores compared with wild-type (WT) mice, despite anti-collagen antibody production and complement activation similar to WT mice. IP−/− mice also showed significant reduction in contents of proinflammatory cytokines, such as interleukin (IL)-6 in arthritic paws. Consistently, the addition of an IP agonist to cultured synovial fibroblasts significantly enhanced IL-6 production and induced expression of other arthritis-related genes. On the other hand, loss or inhibition of each PGE receptor subtype alone did not affect elicitation of inflammation in CIA. However, a partial but significant suppression of CIA was achieved by the combined inhibition of EP2 and EP4. Our results show significant roles of both PGI2-IP and PGE2-EP2/EP4 signaling in the development of CIA, and suggest that inhibition of PGE2 synthesis alone may not be sufficient for suppression of RA symptoms.

scholarly journals Histamine index and clinical expression of rheumatoid arthritis activity

2010 ◽  
Vol 67 (4) ◽  
pp. 286-290 ◽  
Author(s):  
Aleksandra Tomic-Lucic ◽  
Suzana Pantovic ◽  
Gvozden Rosic ◽  
Zdravko Obradovic ◽  
Mirko Rosic
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Disease Activity ◽  
Disease Activity Score ◽  
Joint Destruction ◽  
Clinical Expression ◽  
Histamine Concentration ◽  
Significant Difference ◽  
Rheumatoid Arthritis Activity

Background/Aim. Many arguments prove the pathophysiologic role of histamine in the process of remodeling and joint destruction in rheumatoid arthritis. The aim of our study was to find out if there was a relation between histamine concentration in synovial fluid and blood with clinical expression of disease activity. Methods. Histamine concentration in synovial fluid and blood was determinated in 19 patients with rheumatoid arthritis. Histamine concentration measurement was based on the Shore's fluorometric method. Histamine index (HI) was evaluated as a ratio between histamine concentration in synovial fluid and blood. Disease activity score, DAS 28 (3), with three variables (erythrocyte sedimentation rate, the number of swelled joints and the number of tender joints) was also evaluated. Results. Our results showed that there was no significant difference in concentration of histamine in synovial fluid and blood related to disease activity. However, there was a significant difference in the histamine index which was increased proportionally with disease activity. Conclusion. Our study indicates that histamine index could be useful in estimation of rheumatoid arthritis activity.

scholarly journals Citrullinated vimentin as an important antigen in immune complexes from synovial fluid of rheumatoid arthritis patients with antibodies against citrullinated proteins

2010 ◽  
Vol 12 (4) ◽  
pp. R132 ◽  
Author(s):  
Katleen Van Steendam ◽  
Kelly Tilleman ◽  
Marlies De Ceuleneer ◽  
Filip De Keyser ◽  
Dirk Elewaut ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Immune Complexes ◽  
Citrullinated Proteins ◽  
Citrullinated Vimentin

scholarly journals Inhibition of Interleukin 10 Signaling after Fc Receptor Ligation and during Rheumatoid Arthritis

2003 ◽  
Vol 197 (11) ◽  
pp. 1573-1583 ◽  
Author(s):  
Jong-Dae Ji ◽  
Ioannis Tassiulas ◽  
Kyung-Hyun Park-Min ◽  
Ani Aydin ◽  
Ingrid Mecklenbräuker ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Complexes ◽  
Inflammatory Responses ◽  
Fc Receptors ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Fc Receptor ◽  
Receptor Expression ◽  
Inflammatory Factors

Interleukin-10 (IL-10) is a potent deactivator of myeloid cells that limits the intensity and duration of immune and inflammatory responses. The activity of IL-10 can be suppressed during inflammation, infection, or after allogeneic tissue transplantation. We investigated whether inflammatory factors suppress IL-10 activity at the level of signal transduction. Out of many factors tested, only ligation of Fc receptors by immune complexes inhibited IL-10 activation of the Jak-Stat signaling pathway. IL-10 signaling was suppressed in rheumatoid arthritis joint macrophages that are exposed to immune complexes in vivo. Activation of macrophages with interferon-γ was required for Fc receptor–mediated suppression of IL-10 signaling, which resulted in diminished activation of IL-10–inducible genes and reversal of IL-10–dependent suppression of cytokine production. The mechanism of inhibition involved decreased cell surface IL-10 receptor expression and Jak1 activation and was dependent on protein kinase C delta. These results establish that IL-10 signaling is regulated during inflammation and identify Fc receptors and interferon-γ as important regulators of IL-10 activity. Generation of macrophages refractory to IL-10 can contribute to pathogenesis of inflammatory and infectious diseases characterized by production of interferon-γ and immune complexes.

Differential diagnosis between rheumatoid arthritis and psoriatic arthritis: the value of ultrasound findings at metacarpophalangeal joints level

2011 ◽  
Vol 70 (6) ◽  
pp. 1111-1114 ◽  
Author(s):  
Marwin Gutierrez ◽  
Emilio Filippucci ◽  
Fausto Salaffi ◽  
Luca Di Geso ◽  
Walter Grassi
Keyword(s):  
Rheumatoid Arthritis ◽  
Differential Diagnosis ◽  
Psoriatic Arthritis ◽  
Synovial Fluid ◽  
Potential Role ◽  
Power Doppler ◽  
Extensor Tendon ◽  
Synovial Hypertrophy ◽  
Ultrasound Findings

ObjectiveTo investigate the potential of ultrasound (US) in the differential diagnosis between rheumatoid arthritis (RA) and psoriatic arthritis (PsA) at metacarpophalangeal (MCP) joints level.Methods18 RA patients and 20 PsA patients with clinical involvement of MCP joints were included. All US examinations were performed by two rheumatologists investigating: presence of joint cavity widening (JCW), synovial fluid and/or synovial hypertrophy, peritenon extensor tendon inflammation (PTI) and intra-articular or peri-tendinous power Doppler (PD) signal.ResultsA total of 83 MCP joints in 18 RA patients were assessed. In all of these the authors found different degrees of JCW. 15 of 83 (18%) MCP joints showed synovial fluid, whereas 68 of 83 (82%) MCP joints showed synovial hypertrophy. In 72 of 83 (86.7%) MCP joints intra-articular PD was detected. No PTI pattern was found in these patients.In PsA patients, a total of 82 MCP joints in 20 patients were assessed. 54 of 82 (65.8%) MCP joints showed PTI pattern (p = 0.001). In 50 of these 54 (92.5%) MCP joints extra-articular PD signal was detected (p = 0.001). 28 of 82 (34.1%) MCP joints showed different degrees of JCW. 6 of 28 (21.4%) MCP joints presented synovial fluid, whereas 22 of 28 (78.5%) MCP joints showed synovial hypertrophy. In 8 of 82 (9.7%) MCP joints the JCW and PTI patterns were found contemporaneously.ConclusionsPreliminary results demonstrate that PTI pattern is a higher characteristic of PsA, which suggests a potential role of US in the differential diagnosis between RA and PsA at MCP joints level.

Rheumatoid Arthritis: Pathophysiology

1999 ◽  
Vol 12 (4) ◽  
pp. 282-292 ◽  
Author(s):  
Walter F. Stanaszek ◽  
Bruce C. Carlstedt
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Cells ◽  
Environmental Factors ◽  
Immune Complexes ◽  
Disease Process ◽  
Signs And Symptoms ◽  
Diagnostic Parameters

This article reviews the incidence, etiology, and pathophysiology of rheumatoid arthritis (RA), along with signs and symptoms, laboratory, and other diagnostic parameters of the disease. Criteria utilized for defining RA are discussed. While the primary cause is unknown, theories implicate genetic, hormonal, viral, bacterial, autoimmune, atmospheric, and environmental factors. Recent studies focus on the role of immune complexes, endothelial cells, and antibodies in the disease process.

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