Soluble interleukin-2 receptor, interleukin-2 and interleukin-4 in sera and supernatants from patients with progressive systemic sclerosis

Famularo, Giuseppe; Procopio, Antonio Domenico; Giacomelli, Roberto; Danese, C; Sacchetti, Silvana; Perego, M A; Santoni, Angela; Tonietti, G

doi:10.1111/j.1365-2249.1990.tb05340.x

Cited by 68 publications

(15 citation statements)

References 34 publications

(11 reference statements)

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“…The possibility that differences in T lymphocyte subpopulations in the separated mononuclear cell samples might explain some ofthe observed differenees also has to be eonsidered, but we and others [47], have found no significant differences compared with normal controls in the disease groups we have studied. While there is evidence of an impaired IFN-y produetion by T lymphocytes and, eonsequently, serum IFN-y levels are low in PSS [48], other serum markers of lymphoeyte aetivation are elevated, sueh as IL-2, soluble IL-2 receptors [49] and soluble CD8 [50]. This suggests a selective deficiency of activated lymphocytes to seerete IFN-y.…”

Section: Discussionmentioning

confidence: 99%

In vivo levels and in vitro production of interferon-gamma in fibrosing interstitial lung diseases

C¹,

Haslam²

1992

Clinical and Experimental Immunology

108

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SUMMARY The in vivo role of interferons in the development of fibrosis is not fully understood but it is known that interferons can suppress fibroblast proliferation and collagen synthesis in vitro. We have recently demonstrated that in a group of patients with sarcoidosis having predominant pulmonary involvement, patients with the highest levels of circulating interferon‐gamma (IFN‐y) more frequently resolved on corticosteroids, suggesting that they had a less‘fibrotic’ component to their disease. We now report that in two other diseases, where the tendency to develop pulmonary fibrosis is greater than in sarcoidosis, namely cryptogenic fibrosing alveolitis (CFA) and fibrosing alveolitis associated with the systemic connective tissue disease progressive systemic sclerosis (FA + PSS), very few patients have elevations in IFN‐γ in their serum. However, as in sarcoidosis, those with the highest levels responded to corticosteroids (P < 0·05). Attempts to measure IFN‐γ levels in the lungs, using cell‐free bronchoalveolar lavage (BAL) fluid supernatants, were negative in all the study groups, suggesting that these samples may be inadequate for such studies. To investigate whether there might be an intrinsic defect in T lymphocyte function associated with predisposition to fibrosing lung diseases, we then investigated the in vitro production of IFN‐y by lymphocytes separated from the blood of 18 untreated patients (six with CFA, six with FA + PSS and six with sarcoidosis). IFN‐γ production was impaired in 10 (56%) (two with CFA, four with FA + PSS and four with sarcoidosis). A higher proportion of the fibrosing alveolitis patients (CFA or FA + PSS) with impaired IFN‐γ production have subsequently shown spontaneous lung functional deterioration. These findings suggest that impaired IFN‐γ release might be a potentiating factor in the pathogenesis of these fibrosing lung diseases.

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Section: Discussionmentioning

confidence: 99%

In vivo levels and in vitro production of interferon-gamma in fibrosing interstitial lung diseases

C¹,

Haslam²

1992

Clinical and Experimental Immunology

108

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“…Furthermore, an altered balance between T helper type (Th)1 and Th2 cytokines towards a Th2-polarised immune response plays a pivotal role in SSc 6. Indeed, several growth factors, profibrotic Th2-associated cytokines and chemokines have been implicated in the pathogenesis of SSc including transforming growth factor β, platelet-derived growth factor, connective tissue growth factor, interleukin 4 (IL4), IL13, monocyte chemoattractant protein-1 and endothelin-1 1 2 6–8…”

Section: Introductionmentioning

confidence: 99%

The IL1-like cytokine IL33 and its receptor ST2 are abnormally expressed in the affected skin and visceral organs of patients with systemic sclerosis

et al. 2009

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“…During the disease process, activated macrophages and T cells accumulate in the lungs, and several cytokines and growth factors become elevated in the bloodstream (6)(7)(8)(9)(10)(11) and bronchoalveolar lavage fluid (BALF) (12). Increases in IL-1 and TNF-a may be the result of generalized inflammation, but increases in several other cytokines, including IL-4, IL-13, transforming growth factor-b, and monocyte chemotactic protein (MCP)-1, may be the primary mediators of the scleroderma disease process (3,4).…”

mentioning

confidence: 99%

Resistin-Like Molecule-β in Scleroderma-Associated Pulmonary Hypertension

Angelini¹,

Su²,

Yamaji-Kegan³

et al. 2009

Am J Respir Cell Mol Biol

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Scleroderma is a systemic, mixed connective tissue disease that can impact the lungs through pulmonary fibrosis, vascular remodeling, and the development of pulmonary hypertension and right heart failure. Currently, little is known about the molecular mechanisms that drive this condition, but we have recently identified a novel gene product that is up-regulated in a murine model of hypoxia-induced pulmonary hypertension. This molecule, known as hypoxia-induced mitogenic factor (HIMF), is a member of the newly described resistin gene family. We have demonstrated that HIMF has mitogenic, angiogenic, vasoconstrictive, inflammatory, and chemokine-like properties, all of which are associated with vascular remodeling in the lung. Here, we demonstrate that the human homolog of HIMF, resistin-like molecule (RELM)-b, is expressed in the lung tissue of patients with scleroderma-associated pulmonary hypertension and is up-regulated compared with normal control subjects. Immunofluorescence colocalization revealed that RELM-b is expressed in the endothelium and vascular smooth muscle of remodeled vessels, as well as in plexiform lesions, macrophages, T cells, and myofibroblastlike cells. We also show that addition of recombinant RELM-b induces proliferation and activation of ERK1/2 in primary cultured human pulmonary endothelial and smooth muscle cells. These results suggest that RELM-b may be involved in the development of scleroderma-associated pulmonary hypertension.

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Soluble interleukin-2 receptor, interleukin-2 and interleukin-4 in sera and supernatants from patients with progressive systemic sclerosis

Cited by 68 publications

References 34 publications

In vivo levels and in vitro production of interferon-gamma in fibrosing interstitial lung diseases

In vivo levels and in vitro production of interferon-gamma in fibrosing interstitial lung diseases

The IL1-like cytokine IL33 and its receptor ST2 are abnormally expressed in the affected skin and visceral organs of patients with systemic sclerosis

Resistin-Like Molecule-β in Scleroderma-Associated Pulmonary Hypertension

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