Expression of tumor necrosis factor-receptor superfamily members by lung T lymphocytes in interstitial lung disease.

Agostini, Carlo; Zambello, Renato; Sancetta, Rosaria; Cerutti, Andrea; Milani, A.; Tassinari, Cristina; Facco, Monica; Cipriani, A; Trentin, Livio; Semenzato, Gianpietro

doi:10.1164/ajrccm.153.4.8616567

Cited by 61 publications

(40 citation statements)

References 16 publications

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“…In addition to granuloma formation, pulmonary sarcoid disease is characterized by the expansion of Th1 cells in the lung due to a cellular redistribution from the peripheral blood (19 -22). This lymphocytosis is controlled by chemoattractant cytokines which cooperate to expand the intraalveolar pool of CD4 ϩ T cells within the inflamed area (25,53,54). In situ IL-2-mediated proliferation further contributes to CD4…”

Section: Discussionmentioning

confidence: 99%

Role of IL-18 in CD4+ T Lymphocyte Activation in Sarcoidosis

Greene

Meachery

Taggart

et al. 2000

The Journal of Immunology

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Sarcoidosis is a granulomatous disease of unknown etiology associated with the expansion of IL-2-producing activated CD4+ T lymphocytes. A number of factors including the recently described IL-18 have been implicated in IL-2 expression in vitro. We investigated the role of IL-18 in IL-2 expression in sarcoidosis. Eighteen individuals with sarcoidosis and 15 normal controls were studied. IL-18R expression and epithelial lining fluid (ELF) concentrations of IL-18 were significantly elevated in the sarcoid group (p = 0.0143 and 0.0024, respectively). Both AP1 and NF-κB, transcription factors that regulate IL-2 gene expression, were activated in vivo in sarcoid pulmonary CD4+ T lymphocytes. Transcription factor activity was not detected in pulmonary CD4+ T lymphocytes from normal controls or from peripheral blood CD4+ T lymphocytes from individuals with sarcoidosis, further evidence of compartmentalization of the lymphoproliferative process in this condition. We examined the effects of IL-18 on AP1 and NF-κB in Jurkat T cells in vitro. These effects were both time and dose dependent. Examination of transcription factor activation and IL-2 gene expression in Jurkat T cells revealed that sarcoid but not normal ELF activated AP1 and NF-κB, induced IL-2 gene transcription, and up-regulated IL-2 protein production. Addition of IL-18 to normal ELF also induced IL-2 mRNA accumulation, whereas correspondent depletion of IL-18 from sarcoid ELF using neutralizing Abs abrogated all of the effects. These data strongly implicate IL-18 in the pathogenesis of sarcoidosis via activation of AP1 and NF-κB, leading to enhanced IL-2 gene expression and IL-2 protein production and concomitant T cell activation.

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Section: Discussionmentioning

confidence: 99%

Role of IL-18 in CD4+ T Lymphocyte Activation in Sarcoidosis

Greene

Meachery

Taggart

et al. 2000

The Journal of Immunology

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“…CD8ϩ T cells from subjects in group 1 had reduced gene expression of TNF family members, the cell surface expression of which is associated with susceptibility to activationinduced cell death (27,(55)(56)(57)(58)(59), with decreased expression of TNF receptor I (TNFRI), TNFRII, TRAILR-1, CD30 ligand, and Fas ( Figure 3C). In contrast, expression of the gene for IL-15R␣ chain was increased, whereas the gene for IL-2R␥ was decreased ( Figure 3C).…”

Section: Cd8ϩ T Cells In Scleroderma Lung Disease 2267mentioning

confidence: 99%

Occurrence of an activated, profibrotic pattern of gene expression in lung CD8+ T cells from scleroderma patients

Luzina¹,

Atamas²,

Wise³

et al. 2003

Arthritis & Rheumatism

108

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Objective. Pulmonary fibrosis is a major cause of death in scleroderma patients. Previous studies have shown an increase in CD8؉ T cells in the lungs of scleroderma patients. In the present study, we sought to determine whether activated CD8؉ T cells contribute to pulmonary fibrosis in scleroderma patients through the production and activation of profibrotic mediators.Methods. CD8؉ cells were isolated from bronchoalveolar lavage fluid obtained from 19 scleroderma patients and 7 healthy subjects. The phenotype of these cells was determined using DNA array technology. Expression of selected genes was confirmed in real-time polymerase chain reaction and enzyme-linked immunosorbent assay experiments.

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“…These receptors can lead to either apoptosis or survival of immune cells when ligated by their corresponding ligands [4]. Some studies have shown the involvement of apoptotic receptors in interstitial lung diseases [5,6].…”

mentioning

confidence: 99%

Expression of tumour necrosis factor receptors by bronchoalveolar cells in hypersensitivity pneumonitis

Chen

Tong²,

Ye³

et al. 2005

Eur Respir J

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Tumour necrosis factor receptors (TNFR) and the Fas receptor (FasR) have been implicated in the pathogenesis of interstitial lung diseases. The current authors examined the expression of TNFR-1, TNFR-2 and FasR by bronchoalveolar cells in hypersensitivity pneumonitis (HP).Cell surface receptor expression on bronchoalveolar lavage cells was analysed by immunocytochemistry in 11 HP patients, 11 idiopathic pulmonary fibrosis (IPF) patients and 10 controls.TNFR-1, TNFR-2 and FasR were expressed on a higher percentage of alveolar macrophages (AM) in HP compared with controls and IPF patients. TNFR-2 and FasR expression on lymphocytes was also higher in HP than in controls and in IPF. TNFR-1, TNFR-2 and FasR expression correlated positively with the percentage of lymphocytes, and negatively with the percentage of AM in HP. Expression of TNFR-1 on AM and TNFR-2 on lymphocytes correlated with the percentage of neutrophils in HP.In conclusion, this study shows evidence of altered expression of tumour necrosis factor superfamily receptors in hypersensitivity pneumonitis.

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Expression of tumor necrosis factor-receptor superfamily members by lung T lymphocytes in interstitial lung disease.

Cited by 61 publications

References 16 publications

Role of IL-18 in CD4+ T Lymphocyte Activation in Sarcoidosis

Role of IL-18 in CD4+ T Lymphocyte Activation in Sarcoidosis

Occurrence of an activated, profibrotic pattern of gene expression in lung CD8+ T cells from scleroderma patients

Expression of tumour necrosis factor receptors by bronchoalveolar cells in hypersensitivity pneumonitis

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