Southwestern Internal Medicine Conference: Clinical Features, Pathogenic Mechanisms, and New Developments in the Treatment of Systemic Sclerosis

Geppert, Tom

doi:10.1097/00000441-199003000-00009

Cited by 24 publications

(5 citation statements)

References 124 publications

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“…The role of IL-4 and IL-1 3 in stimulating IL-6 in epidermal cells may be directly relevant in vivo in autoimmune skin diseases such as scleroderma [24] and psoriasis [25] where overproduction of IL-6 has been implicated and activated T-cell infiltrates with a helperinducer phenotype have been observed [1, 26,27]. Thus IL-4 and IL-13 which both are products of helper Tcells, may be directly involved in the pathogenesis of these diseases by locally increasing the IL-6 production in affected sites.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

Derocq¹,

Ségui²,

Poinot-Chaze³

et al. 1994

FEBS Letters

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Interleukin-13 (IL-13) is a recently described human lymphokine which is produced by activated T-cells. Its effect on the production of IL-6 by normal keratinocytes and keratinocyte cell lines of human origin was studied and compared to that of IL-4. IL-13, similarly to IL-4, stimulated IL-6 expression by these cells in a dose-and time-dependent manner. Contamination with endotaxin was excluded by the use of polymyxin B and heat-inactivated cytokines. Further, we showed that IL-13, like IL-4, not only stimulated IL-6 production but also was able to induce overexpression of this cytokine in response to an inflammatory signal such as lipopolysaccharide (LPS). In a previous study, we demonstrated that IL-1 3, by inhibiting IL-6 and other cytokines produced by monocytes, exhibited an ~anti-in~ammato~ profile' comparable to that displayed by IL-4, In contrast, we show here that IL-B, by stimulating IL-4 production by keratinocytes, may favour the instaIlation of an ~~~ato~ process at a local level and, here again, it acted like IL-4. Therefore, according to the type of target cell, these two 'TH2 type' cytokines induce similar opposing effects on IL-6 production and are likely to be important cytokines in the regulation of inflation at bath systemic and 1ocaI levels.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

Derocq¹,

Ségui²,

Poinot-Chaze³

et al. 1994

FEBS Letters

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“…lymphocytes, monocytes, platelets and mast cells) infiltrate the SSc lesion, especially in the early stage of the disease. These cells produce cytokines and growth factors regulating the population of fibroblasts that synthesize large amounts of collagen, 2,3 suggesting that the regulation of pro‐ and anti‐inflammatory processes may be a potent treatment for SSc.…”

Section: Introductionmentioning

confidence: 99%

9-Cis-retinoic acid exhibits antifibrotic activity via the induction of cyclooxygenase-2 expression and prostaglandin E₂production in scleroderma fibroblasts

et al. 2008

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In vitro, 9-cis-RA induced COX-2 expression and PGE(2) production in SSc fibroblasts and PGE(2) downregulated CTGF expression, leading to the inhibition of type I and III collagen synthesis. Our results indicate that the clinical effects of 9-cis-RA on SSc are, at least in part, attributable to the induction of PGE(2) and the subsequent suppression of CTGF expression that results in the blockade of collagenogenesis.

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“…Pulmonary involvement ranks after the skin, peripheral vasculature and esophagus in prevalence (7). Pulmonary involvement ranks after the skin, peripheral vasculature and esophagus in prevalence (7).…”

mentioning

confidence: 99%

“…Systemic sclerosis (SSc) is a multisystem disorder characterized by vascular obliteration and fibrosis of the skin and internal organs. Pulmonary involvement ranks after the skin, peripheral vasculature and esophagus in prevalence (7). Presence of interstitial lung disease constitutes one of the American Rheumatism Association (ARA) preliminary criteria for the disease (21).…”

mentioning

confidence: 99%

Interstitial lung disease in systemic sclerosis: An HRCT-clinical correlative study

et al. 2003

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Southwestern Internal Medicine Conference: Clinical Features, Pathogenic Mechanisms, and New Developments in the Treatment of Systemic Sclerosis

Cited by 24 publications

References 124 publications

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

9-Cis-retinoic acid exhibits antifibrotic activity via the induction of cyclooxygenase-2 expression and prostaglandin E₂production in scleroderma fibroblasts

Interstitial lung disease in systemic sclerosis: An HRCT-clinical correlative study

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Southwestern Internal Medicine Conference: Clinical Features, Pathogenic Mechanisms, and New Developments in the Treatment of Systemic Sclerosis

Cited by 24 publications

References 124 publications

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

Interleukin‐13 stimulates interleukin‐6 production by human keratinocytes

9-Cis-retinoic acid exhibits antifibrotic activity via the induction of cyclooxygenase-2 expression and prostaglandin E2production in scleroderma fibroblasts

Interstitial lung disease in systemic sclerosis: An HRCT-clinical correlative study

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9-Cis-retinoic acid exhibits antifibrotic activity via the induction of cyclooxygenase-2 expression and prostaglandin E₂production in scleroderma fibroblasts