Mostrar el registro sencillo del ítem
T-cells and B-cells in systemic sclerosis
dc.creator | Sakkas, L. I. | en |
dc.creator | Platsoucas, C. D. | en |
dc.date.accessioned | 2015-11-23T10:46:49Z | |
dc.date.available | 2015-11-23T10:46:49Z | |
dc.date.issued | 2010 | |
dc.identifier | 10.2174/157339710793205657 | |
dc.identifier.issn | 15733971 | |
dc.identifier.uri | http://hdl.handle.net/11615/32802 | |
dc.description.abstract | Systemic sclerosis (SSc) is characterized by activation of fibroblasts with extensive deposition of collagen, by small vessel vasculopathy with fibrointimal proliferation, and activation of the immune system, with hyper-γ- globulinaemia and autoantibodies. Twin studies have shown that genetic factors play a minor role in SSc development. Serum autoantibodies and skin lymphocytic infiltrates and small vessel damage occur very early before the appearance of skin fibrosis. T cells can cause fibrosis and vasculopathy through cell-cell contact and cytokines. They produce TH2 cytokines (IL-4, IL13) and TH17 cytokines (IL-17), which are profibrotic. TH2 cells in experimental models also induce pulmonary arterial hypertension. Genetically engineered TGFβ expression in pig arteries causes fibrointimal proliferation. T cells in skin lesions exhibit oligoclonality that persists over time, which indicates an antigen-driven T cell activation, but the antigen(s) responsible are not known. There are known environmental factors that can elicit an immune response and cause a SSc-like disease. T cells also provide help for B cells. B cells can contribute to fibrosis and vasculopathy through cytokines and autoantibodies. Autoantibodies can activate endothelial cells and fibroblasts to a profibrotic phenotype. Finally, treatments directed against T cells and B cells show promising effects in SSc. © 2010 Bentham Science Publishers Ltd. | en |
dc.source.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-78649360435&partnerID=40&md5=64cffc7bebde5c9100fc626bd1e5052e | |
dc.subject | Autoantibodies | en |
dc.subject | B-cells | en |
dc.subject | Systemic sclerosis | en |
dc.subject | T-cells | en |
dc.subject | bleomycin | en |
dc.subject | interleukin 13 | en |
dc.subject | interleukin 17 | en |
dc.subject | interleukin 4 | en |
dc.subject | transforming growth factor beta | en |
dc.subject | antibody blood level | en |
dc.subject | article | en |
dc.subject | B lymphocyte | en |
dc.subject | cell infiltration | en |
dc.subject | cell interaction | en |
dc.subject | chronic graft versus host disease | en |
dc.subject | drug induced disease | en |
dc.subject | environmental factor | en |
dc.subject | genetic engineering | en |
dc.subject | heredity | en |
dc.subject | human | en |
dc.subject | immune response | en |
dc.subject | lymphocyte proliferation | en |
dc.subject | nonhuman | en |
dc.subject | pathogenesis | en |
dc.subject | phenotype | en |
dc.subject | priority journal | en |
dc.subject | protein expression | en |
dc.subject | pulmonary hypertension | en |
dc.subject | skin fibrosis | en |
dc.subject | T lymphocyte | en |
dc.subject | T lymphocyte activation | en |
dc.subject | Th17 cell | en |
dc.subject | Th2 cell | en |
dc.subject | vascular disease | en |
dc.title | T-cells and B-cells in systemic sclerosis | en |
dc.type | journalArticle | en |
Ficheros en el ítem
Ficheros | Tamaño | Formato | Ver |
---|---|---|---|
No hay ficheros asociados a este ítem. |