ArticleArthritis research & therapy2005
Expression of cytokine mRNA and protein in joints and lymphoid organs during the course of rat antigen-induced arthritis.
Article in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Neuronal FcγRI mediates acute and chronic joint pain.The Journal of clinical investigation · 2019Article
- Optimization of Folate-Targeted Immunotherapy for the Treatment of Experimental Arthritis.Inflammation · 2016Article
- A new strategy to deliver synthetic protein drugs: self-reproducible biologics using minicircles.Scientific reports · 2014Article
- Evaluation of the novel folate receptor ligand [18F]fluoro-PEG-folate for macrophage targeting in a rat model of arthritis.Arthritis research & therapy · 2013Article
- (Auto)immunity to cartilage matrix proteins - a time bomb?Arthritis research & therapy · 2013Article
- Cytokines profiling by multiplex analysis in experimental arthritis: which pathophysiological relevance for articular versus systemic mediators?Arthritis research & therapy · 2012Article
- The acute inflammatory response to intranigral α-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation.Journal of neuroinflammation · 2011Article
- Interleukin-1β and interleukin-6 in arthritis animal models: roles in the early phase of transition from acute to chronic inflammation and relevance for human rheumatoid arthritis.Molecular medicine (Cambridge, Mass.)Review
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8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokine expression was assessed during antigen-induced arthritis (AIA) in synovial membrane (SM), inguinal lymph node (LN), and spleen using competitive RT-PCR and sandwich ELISA. In the SM, early elevations of IL-1beta and IL-6 mRNA (by 6 hours; 450- and 200-fold, respectively) correlated with the joint swelling; a 6-fold increase in tumor necrosis factor alpha (TNFalpha) was not significant. Not only IL-2 and IFN-gamma (which increased 10,000-fold and 200-fold, respectively), but also IL-5 and IL-10, increased acutely (6 hours - day 1; 3-fold and 35-fold, respectively) in the SM. In general, the protein levels in the SM for IL-1beta, IL-6, TNFalpha, IFN-gamma, IL-4, and IL-10 (increase from 4-fold to 15-fold) matched the course of mRNA expression. In the inguinal LN, there were early mRNA elevations of IL-6 (a 2.5-fold increase by 6 hours, which correlated positively with the joint swelling) and IL-2 (4-fold by 6 hours), as well as later rises of IL-4 and IL-5 (2.5- and 4-fold, respectively, by day 3). No significant elevations of the corresponding proteins in this tissue were observed, except for IL-1beta (by day 6) and IL-10 (by day 1). In the spleen, there were significant mRNA elevations at 6 hours of IL-1beta (1.5-fold), IL-6 (4-fold; positively correlated with the joint swelling), IFN-gamma (3-fold), and IL-2 (7- to 10-fold). IL-5 and IL-10 (2- and 3-fold, respectively) peaked from 6 hours to day 3 in the spleen. Increases of the corresponding proteins were significant in comparison with day 0 only in the case of IL-2 (day 6). By day 6 (transition to the chronic phase), the mRNA for cytokines declined to or below prearthritis levels in all the tissues studied except for IL-1beta in the SM and IL-6 in the spleen. AIA is thus characterized by four phenomena: early synovial activation of macrophages, T helper (Th)1-like, and Th2-like cells; late, well-segregated Th2-like responses in the inguinal LN; late, overlapping Th1-like/Th2-like peaks in the spleen; and chronic elevation of synovial IL-1beta mRNA and spleen IL-6 mRNA.
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