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1.
J Surg Res ; 233: 74-81, 2019 01.
Artículo en Inglés | MEDLINE | ID: mdl-30502290

RESUMEN

BACKGROUND: Human lung transplantation has evolved to an established treatment for pulmonary diseases in their end stages; however, the long-term outcome is worse when compared to all other solid transplantable organs. The major reason for this unfavorable outcome is rejection, either in its acute or chronic form, the latter termed as chronic lung allograft dysfunction. METHODS: A systematic review search was performed. RESULTS: One of the most important immune cells responsible for rejection are T cells. Beside alloreactive CD8+ T cells, CD4+ T cells play a key role during the evolvement of allograft rejection. Certain subsets of these allograft CD4+ T cells have been identified which have been shown to exert either transplant-protective or transplant-injuring properties. These effects have been proven in various experimental models, mainly in rats and mice, and allowed for the gain of important insights into these proinflammatory and anti-inflammatory characteristics including their targetability: while the subsets Th1, Th17, Th22, and Tfh cells have been shown to act in a rather proinflammatory way, Tregs, Th2, and Th9 subsets exert anti-inflammatory effects. Chronic airway obstruction is mainly induced by IL17 as shown across models. CONCLUSIONS: This review shall summarize and provide an overview of the current evidence about the role and effects of proinflammatory and anti-inflammatory CD4-+ T helper cell subsets during lung allograft rejection in experimental rodent models.


Asunto(s)
Rechazo de Injerto/inmunología , Trasplante de Pulmón/efectos adversos , Subgrupos de Linfocitos T/inmunología , Linfocitos T Colaboradores-Inductores/inmunología , Animales , Modelos Animales de Enfermedad , Macaca fascicularis , Ratones , Ratas
3.
Oncotarget ; 9(70): 33440, 2018 09 07.
Artículo en Inglés | MEDLINE | ID: mdl-30279972

RESUMEN

[This corrects the article DOI: 10.18632/oncotarget.22579.].

4.
Artículo en Inglés | MEDLINE | ID: mdl-28290005

RESUMEN

OPINION STATEMENT: Tricuspid regurgitation is frequent and is most often caused by annular dilatation and leaflet tethering from adverse right ventricular remodeling in response to several disease processes (functional tricuspid regurgitation), while primary/organic tricuspid valve regurgitation is less common. Surgical intervention for tricuspid regurgitation is usually performed concomitantly to left-sided heart valve surgery. In isolated significant tricuspid regurgitation, however, many patients are left unoperated as they commonly are considered at very high or prohibitive surgical risk. Moreover, the risk versus benefit data are not as well-established as compared to other valve disease. Multiple novel transcatheter therapies have now begun to emerge with the aim to treat tricuspid regurgitation less invasively. For most new interventional procedures, current trials are designed to prove efficacy and safety. In the foreseeable future, however, patients with significant MR can likely be offered a multifaceted palette of minimally invasive transcatheter options in addition to conventional surgery, which will allow to treat more patients in need. These current developments make tricuspid valve disease and its therapy an exciting field of study.

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