Título:	Turning up the heat : inflammasome activation by fungal pathogens
Autor(es):	Tavares, Aldo Henrique Fonseca Pacheco Bürgel, Pedro Henrique Bocca, Anamélia Lorenzetti
Assunto:	Doenças transmissíveis Fungos Proteínas Inflamassoma Imunologia
Data de publicação:	23-Jul-2015
Editora:	Plos One
Referência:	TAVARES, Aldo Henrique; BÜRGEL, Pedro Henrique; BOCCA, Anamélia Lorenzetti. Turning up the heat: inflammasome activation by fungal pathogen. Plos Pathogens, v. 11, n. 7, Article e1004948, 23 jul. 2015. Disponível em: <http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004948>. Acesso em: 22 jun. 2017. doi: 10.1371/journal.ppat.1004948.
Abstract:	Since its first description in 2002 [1], the inflammasome has been implicated in the mechanisms underlying a growing number of infectious, autoimmune, and metabolic diseases [2]. Regarding infectious processes, several studies have shown the involvement of this critical component of innate immunity in the outcome of infection with nearly every class of microbe, including fungi [3]. Innate immunity is the frontline of defense against infection and relies on the ability of its main players (phagocytes and epithelial barriers) to detect conserved components of microbes or pathogen-associated molecular patterns (PAMPs). In fungi, the carbohydrate polymers of the cell wall, such as chitin, β-glucan, and mannan are the major PAMPs recognized by the host’s innate immune cells; this recognition occurs via germline-encoded receptors termed pattern recognition receptors (PRRs) [4]. In addition to PAMPs, endogenous molecules associated with damaged host cells, or damage-associated molecular patterns (DAMPs), are released during tissue injury and activate PRRs. This innate detection system includes the Toll-like receptors (TLRs), C-type lectin receptors (CLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), and AIM2-like receptors (ALRs). Although the main fungal- recognition PRRs (CLRs and TLRs) are bound to the cytoplasmic membrane of innate immune cells [4], fungal sensing by PRRs located in the cytosol, such as the NLRs and ALRs, is becoming increasingly evident. A number of NLRs and ALRs can assemble into the inflammasome, a multiprotein complex consisted of PRRs such as NLRP3 (NLR family, pyrin domain-containing 3), NLRC4, or AIM2, adaptor protein ASC (apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (CARD), and procaspase-1 [3]. Upon formation of the complex, procaspase-1 is cleaved into an active cysteine protease, which further cleaves the proinflammatory cytokines IL-1β and IL-18 into their mature forms, followed by unconventional secretion. IL-1β and IL-18 mediate several innate antimicrobial responses and are critical to direct adaptive Th17/Th1 cellular responses [5]. In addition, inflammasome activation causes pyroptosis, a lytic inflammatory form of cell death [2,5].
Licença:	Copyright: © 2015 Tavares et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
DOI:	https://dx.doi.org/10.1371/journal.ppat.1004948
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