T lymphocytes synthesize and export heparin-binding epidermal growth factor-like growth factor and basic fibroblast growth factor, mitogens for vascular cells and fibroblasts: differential production and release by CD4+ and CD8+ T cells.

Blotnick, Srully; Peoples, George E.; Freeman, Michael R.; Eberlein, Timothy J.; Klagsbrun, Michael

doi:10.1073/pnas.91.8.2890

Cited by 287 publications

(177 citation statements)

References 27 publications

Supporting

Mentioning

166

Contrasting

Unclassified

Order By: Relevance

“…However, we were unable to demonstrate any differences compared with animals treated with control antibody, which might indicate that other growth factors could be more important in the induction of epithelial hypertrophy. Nevertheless, our observations do not exclude a role for EGFR ligands produced by macrophages (Madtes et al, 1988), by eosinophils (Brach et al, 1994), or by T cells themselves (Blotnik et al, 1994) in the pathogenesis of subepithelial fibrosis.…”

Section: Foster Et Almentioning

confidence: 71%

CD4+ T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

Foster

Yang

Herbert

et al. 2002

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY:Asthma is an acute-on-chronic inflammatory disease of the airways, characterized by airflow obstruction and hyper-reactivity of the airways to a variety of stimuli. Chronic asthma is associated with remodeling of the airway wall, which may contribute to hyper-reactivity and fixed airflow obstruction. We used an improved mouse model of chronic asthma to investigate the role of CD4 ϩ T-lymphocytes in airway remodeling and hyper-reactivity. Animals functionally depleted of CD4 ϩ T-lymphocytes by repeated administration of a monoclonal antibody exhibited markedly decreased airway responsiveness. In addition, these mice had greatly diminished subepithelial fibrosis, epithelial thickening, and mucous cell hyperplasia/metaplasia. Chronic inflammation in the airway wall was moderately reduced, with a marked decrease in the accumulation of immunoglobulinsynthesizing plasma cells. However, intraepithelial accumulation of eosinophils was not significantly inhibited and airway epithelial expression of eotaxin was undiminished. This work provides the first experimental evidence that CD4 ϩ T-lymphocytes play a crucial role in the pathogenesis of the lesions of chronic asthma and lends support to the notion that functional inhibition of these cells may be an important therapeutic target. (Lab Invest 2002, 82:455-462).

show abstract

Section: Foster Et Almentioning

confidence: 71%

CD4+ T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

Foster

Yang

Herbert

et al. 2002

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…Certainly, this would explain our finding that extensive lymphocytic infiltration of the prostatic tumour stroma is related with strong TP expression by cancer and stromal cells. The pathway by which lymphocytes, or specific subpopulations of lymphocytes, trigger the expression of TP is not clear, although there are reports implicating CD4 positive cells in tumour angiogenesis (Blotnick et al, 1994) and natural killer (NK) cells in complex interactions with angiogenic factors (Melder et al, 1996). Furthermore, a direct association between lymphocytic and macrophage stromal infiltration was noted.…”

Section: Discussionmentioning

confidence: 99%

Thymidine phosphorylase expression in normal, hyperplastic and neoplastic prostates: correlation with tumour associated macrophages, infiltrating lymphocytes, and angiogenesis

et al. 2002

View full text Add to dashboard Cite

Thymidine phosphorylase is an angiogenic factor primarily expressed by cancer cells, stromal cells and tumour-associated macrophages in many human malignancies. These different types of thymidine phosphorylase-expressing cells, however, may have a distinct place in the angiogenic process, and this question was addressed in the present study. A series of 20 normal/ hyperplastic prostate glands and 60 prostate carcinomas was investigated by immunohistochemistry, using specific antibodies for thymidine phosphorylase (P-GF.44C), tumour-associated macrophages (CD68), endothelium (CD31) and prostate specific antigen (ER-PR8). Thymidine phosphorylase expression by normal and hyperplastic epithelial or stromal cells occurred almost exclusively in the context of an intense lymphocytic infiltrate. High thymidine phosphorylase cancer cells and thymidine phosphorylase stromal cells expression was associated with high angiogenesis in prostate carcinomas, and this significant association was extended to include both tumour-associated macrophages and tumour-infiltrating lymphocytes. Thymidine phosphorylase expression and tumour-infiltrating lymphocytes were related inversely with prostate specific antigen reactivity. In conclusion, thymidine phosphorylase is a major angiogenic factor in prostate carcinomas and its up-regulation is likely to occur in the context of a host immune response.

show abstract

“…4). Inflammatory cells, including mononuclear phagocytes [204,205], CD4 + and CD8 + T lymphocytes [206,207], and mast cells [208] can express FGF2. Moreover, osmotic shock and shear stress induce the release of FGF2 from endothelial cells [209,210].…”

Section: Fgf-dependent Angiogenesis and Inflammationmentioning

confidence: 99%

Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis

Presta

Dell’Era

Mitola

et al. 2005

Cytokine & Growth Factor Reviews

1,108

860

View full text Add to dashboard Cite

Fibroblast growth factors (FGFs) are a family of heparin-binding growth factors. FGFs exert their pro-angiogenic activity by interacting with various endothelial cell surface receptors, including tyrosine kinase receptors, heparan-sulfate proteoglycans, and integrins. Their activity is modulated by a variety of free and extracellular matrix-associated molecules. Also, the cross-talk among FGFs, vascular endothelial growth factors (VEGFs), and inflammatory cytokines/chemokines may play a role in the modulation of blood vessel growth in different pathological conditions, including cancer. Indeed, several experimental evidences point to a role for FGFs in tumor growth and angiogenesis. This review will focus on the relevance of the FGF/FGF receptor system in adult angiogenesis and its contribution to tumor vascularization. #

show abstract

T lymphocytes synthesize and export heparin-binding epidermal growth factor-like growth factor and basic fibroblast growth factor, mitogens for vascular cells and fibroblasts: differential production and release by CD4+ and CD8+ T cells.

Cited by 287 publications

References 27 publications

CD4+ T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

CD4+ T-Lymphocytes Regulate Airway Remodeling and Hyper-Reactivity in a Mouse Model of Chronic Asthma

Thymidine phosphorylase expression in normal, hyperplastic and neoplastic prostates: correlation with tumour associated macrophages, infiltrating lymphocytes, and angiogenesis

Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis

Contact Info

Product

Resources

About