Lymphokine stimulation of collagen accumulation.

Johnson, Robert L.; Ziff, Morris

doi:10.1172/jci108455

Cited by 294 publications

(71 citation statements)

References 38 publications

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“…It has already been demonstrated that unspecified lymphocyte products (Johnson & Ziff, 1976;Postlethwaite et al, 1984), unspecified T-cell products (Wahl & Gately, 1983), interleukin-l, which is produced by many cells including T-cells (Goldring & Krane, 1987;Postlethwaite et al, 1988), and transforming growth factor beta, produced by T-cells and macrophages (Roberts et al, 1986;Raghow et al, 1987), influence collagen production by cultured fibroblasts. The depletion of T-cells inhibited the formation of bacterial cell wall-induced hepatic granulomas in vivo (Wahl et al, 1986), and reduced the ability of immune spleen cells to form granulomas around Schistosoma eggs in vitro (Bentley et al, 1982).…”

Section: Resultsmentioning

confidence: 99%

Collagen production by macrophages in tumour encapsulation and dormancy

Vaage

Harlos²

1991

Br J Cancer

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Section: Resultsmentioning

confidence: 99%

Collagen production by macrophages in tumour encapsulation and dormancy

Vaage

Harlos²

1991

Br J Cancer

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“…Moreover, in no case except NGF did growth factors (in low serum) equal or exceed the stimulation observed with high serum. Results with NGF seemed to show equal or slightly greater stimulation with scleroderma than with control (20) or by nonspecific mitogens (21,22), leads to the elaboration of soluble factors, still poorly identified, which modulate fibroblast proliferation and collagen synthesis. The precise role of these immune events in the pathogenesis of scleroderma awaits further investigation.…”

Section: Resultsmentioning

confidence: 99%

Replication and phenotypic expression of control and scleroderma human fibroblasts: responses to growth factors.

LeRoy¹,

Mercurio²,

Sherer³

1982

Proc. Natl. Acad. Sci. U.S.A.

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To explore the mechanism of increased collagen synthesis by scleroderma skin fibroblasts in vitro, control and scleroderma fibroblasts were compared in confluent monolayer cultures growth-arrested by serum deprivation; responses to optimal mitogenic doses of platelet-derived growth factor, fibroblast growth factor, epidermal growth factor and nerve growth factor were compared. Plateletderived growth factor had a selective mitogenic effect on control skdn fibroblasts not observed with scleroderma skin fibroblasts. None of the factors studied had a selective effect on collagen synthesis independent of cell replication; scleroderma and control fibroblasts responded similarly. Therefore, the growth factors studied may not be involved in generating the activated scleroderma fibroblast directly; platelet-derived growth factor may play an indirect role in fibroblast replication in human fibrotic disorders.More than a decade ago, it was observed that fibroblasts from involved skin of patients with scleroderma synthesized increased levels of collagen in vitro (1, 2); today the mechanism remains unknown (3-6). During this period, observations ofthe pathogenesis of scleroderma have focused on vascular and microvascular lesions; on evidence of endothelial damage; on platelet adhesion, aggregation, and release; and on the subsequent activation both of smooth muscle cells to produce the intimal proliferation and of interstitial fibroblasts to produce fibrosis (7-10). A unifying hypothesis would propose the presence offactors released from plasma or platelets which act as stimuli to fibrosis; among such factors, the potent mitogen, plateletderived growth factor (PDGF), is released during endothelial injury and platelet adhesion to the subendothelium (11). Therefore, the influence of PDGF on skin fibroblast collagen synthesis was studied.Endothelial damage and platelet interaction with the exposed subendothelium, resulting in release of platelet-derived mitogenic factors (including PDGF), have been proposed, at least indirectly, to play a role in the evolution of the scleroderma vascular lesion. Events preceding endothelial injury are poorly understood; altered immunity leading to humoral or lymphocyte/monocyte mediators ofinjury has been proposed with supporting evidence (12). If PDGF is the direct mediator of fibroblast activation in scleroderma, the enhanced collagen synthesis of scleroderma fibroblasts should be accompanied by increased cell replication at some stage in the process. Thus, a PDGF mechanism in scleroderma would imply replication offibroblast populations instead of, or in addition to, the selective stimulation ofcollagen synthesis per cell; in earlier studies, increased collagen synthesis per cell was observed in vitro without evidence of increased cell replication (1, 2). If PDGF is the mediator of fibroblast activation in scleroderma, its action should account for the initial observations of increased collagen synthesis per cell.A second characteristic of scleroderma fibroblasts in culture has been ...

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“…Numerous studies examining the interplay between T cells and fibroblasts in the development of tissue fibrosis and fibroproliferative vasculopathy suggest that activated T cells can trigger fibroblast activation both by direct contact and by paracrine action of secreted cytokines (7,(14)(15)(16)(17)(18)(19)(20). On the other hand, chemokines secreted by activated fibroblasts can induce chemotaxis of inflammatory cells, contributing to the amplification of the pathogenetic process (19,21,22).…”

mentioning

confidence: 99%

T cells expressing allograft inflammatory factor 1 display increased chemotaxis and induce a profibrotic phenotype in normal fibroblasts in vitro

Galdo¹,

Jiménez²

2007

Arthritis & Rheumatism

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Objective. Allograft inflammatory factor 1 (AIF-1) was first identified in rat cardiac allografts undergoing chronic rejection. The vasculopathy of chronic allograft rejection is strikingly similar to that seen in patients with systemic sclerosis (SSc). We previously demonstrated AIF-1 expression in inflammatory cells infiltrating skin and lungs from SSc patients, but its role in SSc pathogenesis is unknown. The present study was undertaken to investigate the effects of AIF-1 on T cell migration and production of cytokines capable of modulating normal dermal fibroblast functions.Methods. Stably transfected Jurkat T cells expressing 2 AIF-1 splicing variants were prepared, and their migration toward fibroblast monolayers assayed in Transwell cultures. Cytokine production was assessed by real-time polymerase chain reaction (PCR) and multiplex enzyme-linked immunosorbent assay. Fibroblast gene expression was quantified by real-time PCR, and collagen production by Western blot analysis of culture media.Results. AIF-1 significantly increased Jurkat T cell migration toward fibroblast monolayers. Expression of AIF-1 isoform 2 in Jurkat T cells up-regulated their production of interleukin-4 (IL-4) and IL-17. Conditioned media from AIF-1-expressing clones stimulated synthesis of types I and III collagen and expression of IL-6, transforming growth factor ␤, endothelin receptor, and ␣-smooth muscle actin by normal dermal fibroblasts.Conclusion. These results suggest that AIF-1 may participate in the early pathogenesis of SSc by promoting tissue T cell infiltration and production of cytokines capable of inducing the expression of a fibrotic phenotype in normal fibroblasts.

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Lymphokine stimulation of collagen accumulation.

Cited by 294 publications

References 38 publications

Collagen production by macrophages in tumour encapsulation and dormancy

Collagen production by macrophages in tumour encapsulation and dormancy

Replication and phenotypic expression of control and scleroderma human fibroblasts: responses to growth factors.

T cells expressing allograft inflammatory factor 1 display increased chemotaxis and induce a profibrotic phenotype in normal fibroblasts in vitro

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