Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/341795
Type: Artigo
Title: Regulatory T cells in paracoccidioidomycosis
Author: Calich, Vera L. G.
Mamoni, Ronei L.
Loures, Flávio V.
Abstract: This review addresses the role of regulatory T cells (Tregs), which are essential for maintaining peripheral tolerance and controlling pathogen immunity, in the host response against Paracoccidioides brasiliensis, a primary fungal pathogen. A brief introduction on the general features of Treg cells summarizes their main functions, subpopulations, mechanisms of suppression and plasticity. The main aspects of immunity in the diverse forms of the P. brasiliensis infection are presented, as are the few extant studies on the relevance of Treg cells in the control of severity of the human disease. Finally, the influence of Toll-like receptors, Dectin-1, NOD-like receptor P3 (NLRP3), Myeloid differentiation factor-88 (MyD88), as well as the enzyme indoleamine 2,3 dioxygenase (IDO) on the expansion and function of Treg cells in a murine model of pulmonary paracoccidioidomycosis (PCM) is also discussed. It is demonstrated that some of these components are involved in the negative control of Treg cell expansion, whereas others positively trigger the proliferation and activity of these cells. Finally, the studies here summarized highlight the dual role of Treg cells in PCM, which can be protective by controlling excessive immunity and tissue pathology but also deleterious by inhibiting the anti-fungal immunity necessary to control fungal growth and dissemination
Subject: Paracoccidioides brasiliensis
Country: Estados Unidos
Editor: Taylor & Francis
Rights: Fechado
Identifier DOI: 10.1080/21505594.2018.1483674
Address: https://www.tandfonline.com/doi/full/10.1080/21505594.2018.1483674
Date Issue: 2019
Appears in Collections:FCM - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
2-s2.0-85052075182.pdf1.46 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.