Role of HLA Class II and Cytokine Expression in Rheumatoid Arthritis

Feldmann, Marc; Kissonerghis, Anna-Maija; Buchan, Glenn; Brennan, Fionula M.; Turner, Martin; Haworth, Catherine; Barrett, Kathy; Chantry, David; Ziegler, A; Maini, R. N.

doi:10.3109/03009748809102951

Cited by 11 publications

(7 citation statements)

References 12 publications

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“…The development of arthritis was associated with increased levels of TNF-␣ and IL-6 mRNAs in affected paws and systemic IL-6 production. Both cytokines have been shown to be produced spontaneously by rheumatoid arthritis synovial cells (34)(35)(36)(37). Treatment of arthritic rats with SC-58125 or indomethacin markedly reduced the level of IL-6 mRNA in affected paws.…”

Section: Discussionmentioning

confidence: 99%

Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis.

Anderson¹,

Hauser²,

McGarity³

et al. 1996

J. Clin. Invest.

530

319

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Prostaglandins formed by the cyclooxygenase (COX) enzymes are important mediators of inflammation in arthritis. The contribution of the inducible COX-2 enzyme to inflammation in rat adjuvant arthritis was evaluated by characterization of COX-2 expression in normal and arthritic paws and by pharmacological inhibition of COX-2 activity. The injection of adjuvant induced a marked edema of the hind footpads with coincident local production of PGE 2 . PG production was associated with upregulation of COX-2 mRNA and protein in the affected paws. In contrast, the level of COX-1 mRNA was unaffected by adjuvant injection. TNF-␣ and IL-6 mRNAs were also increased in the inflamed paws as was IL-6 protein in the serum. Therapeutic administration of a selective COX-2 inhibitor, SC-58125, rapidly reversed paw edema and reduced the level of PGE 2 in paw tissue to baseline. Interestingly, treatment with the COX-2 inhibitor also reduced the expression of COX-2 mRNA and protein in the paw. Serum IL-6 and paw IL-6 mRNA levels were also reduced to near normal levels by SC-58125. Furthermore, inhibition of COX-2 resulted in a reduction of the inflammatory cell infiltrate and decreased inflammation of the synovium. Notably, the antiinflammatory effects of SC-58125 were indistinguishable from the effects observed for indomethacin. These results suggest that COX-2 plays a prominent role in the inflammation associated with adjuvant arthritis and that COX-2 derived PGs upregulate COX-2 and IL-6 expression at inflammatory sites. ( J. Clin. Invest. 1996. 97:2672-2679.)

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Section: Discussionmentioning

confidence: 99%

Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis.

Anderson¹,

Hauser²,

McGarity³

et al. 1996

J. Clin. Invest.

530

319

View full text Add to dashboard Cite

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“…A wide variety of cytokines is produced in the joints of patients with rheumatoid arthritis (Feldmann et al, 1988). IL-1 and TNF-a in particular have been implicated in the destruction of the joints in this condition.…”

Section: Introductionmentioning

confidence: 99%

Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

Danis

Franic

Rathjen

et al. 1991

Clinical and Experimental Immunology

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SUMMARYThe effects of GM-CSF, IL-2, IFN-y. TNF-a and IL-6 on the production of IL-I (both secreted and cell associated) and TNF-a by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum-free conditions which minimized background stimulation of monokine production. GM-CSF. IL-2 and TNF-a directly induced the production of cell-associated IL-1 but liUlcornoIL-l or TNF-a secretion. Combination of GM-CSF with !FN-y. IL-2 or TNF-a synergistically enhanced IL-1 secretion and had an additive eflect on cell-associated IL-1 production. Combination of IL-2 with IFN-7 or TNF-a also synergistically enhanced IL-I secretion but theefiect on cell-associated IL-I production was less than additive. GM-CSF synergistically enhaneed TNF-a secretion induced by IFN-y but not by lipopolysaccharide. GM-CSF did not enhanee TNF-a secretion induced by IL-2 or TNF-a. In contrast. IL-2 syncrgisticatly enhanced TNF-a seeretion induced by IFN--/. These results are discussed in relation lo cytokine involvement in rheumatoid arthritis.

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“…The demonstration of significant levels of IL-1 in RA joints [1] has given credence to this concept. The demonstration of significant levels of IL-1 in RA joints [1] has given credence to this concept.…”

Section: Introductionmentioning

confidence: 89%

“…The demonstration of significant levels of IL-1 in RA joints [1] has given credence to this concept. Although the cellular origins of this IL- 1 have not yet been delineated, particularly high amounts of IL-1 were produced by synovial cells [4,5] and by peripheral blood monocytes [6][7][8][9] cultured in vitro. Although the cellular origins of this IL- 1 have not yet been delineated, particularly high amounts of IL-1 were produced by synovial cells [4,5] and by peripheral blood monocytes [6][7][8][9] cultured in vitro.…”

Section: Introductionmentioning

confidence: 89%

The effect of gold treatment on monocyte interleukin-1 production in rheumatoid arthritis

et al. 1990

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Monocyte interleukin-1 (IL-1) production in vitro was studied in 49 patients with rheumatoid arthritis (RA) and 31 controls. Twenty-six of the RA patients were studied prospectively for up to 12 months after beginning chrysotherapy. About half of the patients (group 1) exhibited pretreatment levels of monocyte IL-1 secretion (as measured by bioassay or B-IL-1) significantly higher than that of the controls. Immunoreactive IL-1 (IR-IL-1) levels, however, were similar to controls. Clinical improvement in this group of patients was modest and transient but could be associated with a fall in the level of IL-1 (B-IL-1 and IR-IL-1) secretion. Other RA patients (group 2) appeared to have normal or reduced pretreatment levels of IL-1 secretion. Chrysotherapy resulted in significant clinical improvement within 3 months, and this was associated with an increase in IL-1 (both B-IL-1 and IR-IL-1) secretion by the patients' blood monocytes to normal or supranormal levels. Thus these two groups of RA patients (which differed only in the average duration of disease) had different prognoses in relation to chrysotherapy and the effect of chrysotherapy-induced remission on monocyte IL-1 secretion was opposite. These results suggest that monocyte IL-1 production in vitro reflects changes secondary to the anti-rheumatic effects of chrysotherapy.

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Role of HLA Class II and Cytokine Expression in Rheumatoid Arthritis

Cited by 11 publications

References 12 publications

Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis.

Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis.

Effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-2, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α) and IL-6 on the production of immunoreactive IL-1 and TNF-α by human monocytes

The effect of gold treatment on monocyte interleukin-1 production in rheumatoid arthritis

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