Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies. Significant SFMC responses to additional organisms associated with ReA were also recorded; since there was no serological evidence of preceding infection by these organisms, this finding suggests that these bacteria share common T cell-recognized antigenic epitopes. The corresponding responses by peripheral blood mononuclear cells (PBMC) were much lower and often barely detectable, whereas their responses to PHA were consistently higher than those of SFMC. These results, combined with evidence that bacterial antigens localize in the joint, indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1541893PMC

Publication Analysis

Top Keywords

reactive arthritis
8
mononuclear cells
8
preceding infection
8
synovial lymphocyte
4
lymphocyte recognition
4
recognition organisms
4
organisms trigger
4
trigger reactive
4
arthritis reactive
4
rea
4

Similar Publications

Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by systemic inflammation. While RA primarily affects the joints, its systemic effects may lead to an increased cerebro- and cardiovascular risk. Atherosclerosis of the carotid arteries is a significant risk factor for cerebrovascular events and serves as a surrogate marker for cardiovascular risk.

View Article and Find Full Text PDF

Background: Currently, the pathophysiology of new bone formation in radiographic axial spondyloarthritis (r-axSpA) remains unclear. Cellular elements and their secreted bone turnover markers might be one of the underlying mechanisms that drive the new bone formation. Our study aimed to investigate the role of bone turnover markers in r-axSpA patients with fatty lesions.

View Article and Find Full Text PDF

mtSTAT3 suppresses rheumatoid arthritis by regulating Th17 and synovial fibroblast inflammatory cell death with IL-17-mediated autophagy dysfunction.

Exp Mol Med

January 2025

Lab of Translational ImmunoMedicine, Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

Th17 cells are activated by STAT3 factors in the nucleus, and these factors are correlated with the pathologic progression of rheumatoid arthritis (RA). Recent studies have demonstrated the presence of STAT3 in mitochondria, but its function is unclear. We investigated the novel role of mitochondrial STAT3 (mitoSTAT3) in Th17 cells and fibroblast-like synoviocytes (FLSs) and analyzed the correlation of mitoSTAT3 with RA.

View Article and Find Full Text PDF

Nr4a1 and Nr4a3 redundantly control clonal deletion and contribute to an anergy-like transcriptome in auto-reactive thymocytes to impose tolerance in mice.

Nat Commun

January 2025

Division of Rheumatology, Rosalind Russell and Ephraim P. Engleman Arthritis Research Center, Department of Medicine, University of California, San Francisco, CA, 94143, USA.

The Nr4a nuclear hormone receptors are transcriptionally upregulated in response to antigen recognition by the T cell receptor (TCR) in the thymus and are implicated in clonal deletion, but the mechanisms by which they operate are not clear. Moreover, their role in central tolerance is obscured by redundancy among the Nr4a family members and by their reported functions in Treg generation and maintenance. Here we take advantage of competitive bone marrow chimeras and the OT-II/RIPmOVA model to show that Nr4a1 and Nr4a3 are essential for the upregulation of Bcl2l11/BIM and thymic clonal deletion by self-antigen.

View Article and Find Full Text PDF

Objectives: We previously found that discrepancy between serum amyloid A (SAA) and C-reactive protein (CRP) levels linked to the difference of SAA/CRP ratio in patients with early rheumatoid arthritis, and the ratio varied among different patients. This study aimed to determine why the SAA/CRP ratio differed among different patients.

Methods: The patients (n=466) with most of inflammatory diseases were enrolled.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!