Navegando por Palavras-chave "Macrophage"

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    Avaliação do papel da proteína anti-inflamatória Anexina A1 na regulação do Inflamassoma NLRP3 e nas infecções por Candida Albicans e Candida Auris: estudo in vitro e caracterização do perfil lipidômico
    (Universidade Federal de São Paulo, 2020-07-17) Sanches Junior, José Marcos; Gil, Cristiane Damas [UNIFESP]; http://lattes.cnpq.br/6047408996026135; http://lattes.cnpq.br/2853203620000520; Universidade Federal de São Paulo (UNIFESP)
    Objetivo: Avaliar o papel da AnxA1 na regulação do inflamassoma NLRP3 e na infecção por C. albicans e C. auris em macrófagos e neutrófilos isolados, bem como avaliar o perfil dos lipídios liberados por essas células após a ativação do NLRP3 e nas infecções por Candida spp. Metodologia: Camundongos machos C57BL/6 selvagens (WT) e nocautes para AnxA1 (AnxA1-/- ) receberam injeção intraperitoneal de solução de amido a 1,5% ou carragenina a 0,3% para obtenção de macrófagos e neutrófilos do lavado peritoneal, respectivamente. Essas células foram estimuladas com lipopolissacarídeo (LPS), (por 3 horas), seguida da administração dos agonistas de NLRP3, nigericina (1 hora) ou ATP (30 minutos). Também foi verificado a ação do peptídeo mimético da AnxA1 (Ac2-26) em neutrófilos ativados pelo NLRP3. Para verificar a resposta de neutrófilos em infecções fúngicas, bem como a relação da AnxA1 nestas condições, estas células foram cocultivadas com as cepas de C. albicans e C. auris por 4 horas. Resultados: Nos macrófagos evidenciou-se que a falta de AnxA1 exacerba a liberação de IL-1β após a indução da ativação do inflamassoma NLRP3, bem como acarreta mudanças no perfil lipídico, tendo as ceramidas como os principais lipídios mediadores. A expressão de NLRP3 foi maior em macrófagos AnxA1-/- tratados com nigericina e pontos de colocalização foram verificados entre o inflamassoma NLRP3 e AnxA1, evidenciando a participação dessa proteína na regulação do NLRP3. Em neutrófilos, a AnxA1 endógena demonstrou ser importante para a ativação do NLRP3, uma vez que a liberação de IL-1β foi inferior quando comparado aos WT. A adição do peptídeo Ac2-26 reduziu a liberação de IL-1β pela via de ativação do inflamassoma NLRP3 em neutrófilos WT, mas não reverteu a liberação desta citocina em neutrófilos AnxA1-/- . Potenciais biomarcadores lipídicos relacionados ao estresse e ativação celular, incluindo esfingolipídios específicos e glicerofosfolipídios, foram identificados no sobrenadante dos neutrófilos de ambos genótipos após ativação por nigericina. O tratamento com Ac2-26 aumentou a concentração de fosfatidilserinas e fosfocolinas oxidadas, biomarcadores lipídicos relacionados à via da resolução inflamatória. Neutrófilos AnxA1-/- cocultivados com C. albicans ou C. auris apresentam maior expressão de COX-2 e ativação das MAPKs em relação aos WT. A falta de AnxA1 promoveu diferença no perfil lipídico, tendo maior proeminência de glicerofosfolipídios, tanto em neutrófilos co-infectados quanto no grupo AnxA1-/- controle. Conclusão: A AnxA1 desempenha diferentes papeis na sinalização do inflamassoma NLRP3 com base em sua localização intra ou extracelular e tipo celular. Além disso, regula a ativação dos neutrófilos pela infecção por Candida spp., evidenciando seu potencial imunomodulador em doenças inflamatórias e infecciosas.
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    B-1 cells temper endotoxemic inflammatory responses
    (Elsevier B.V., 2011-03-01) Barbeiro, Denise Frediani; Barbeiro, Hermes Vieira; Faintuch, Joel; Kubo Ariga, Suely K.; Mariano, Mario [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Souza, Heraldo Possolo de; Velasco, Irineu Tadeu; Soriano, Francisco Garcia; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Sepsis syndrome is caused by inappropriate immune activation due to bacteria and bacterial components released during infection. This syndrome is the leading cause of death in intensive care units. Specialized B-lymphocytes located in the peritoneal and pleural cavities are known as B-1 cells. These cells produce IgM and IL-10, both of which are potent regulators of cell-mediated immunity. It has been suggested that B-1 cells modulate the systemic inflammatory response in sepsis. in this study, we conducted in vitro and in vivo experiments in order to investigate a putative role of B-1 cells in a murine model of LPS-induced sepsis. Macrophages and B-1 cells were studied in monocultures and in co-cultures. the B-1 cells produced the anti-inflammatory cytokine IL-10 in response to LPS. in the B-1 cell-macrophage co-cultures, production of proinflammatory mediators (TNF-alpha, IL-6 and nitrite) was lower than in the macrophage monocultures, whereas that of IL-10 was higher in the co-cultures. Co-culture of B-1 IL-10(-/-) cells and macrophages did not reduce the production of the proinflammatory mediators (TNF-alpha, IL-6 and nitrite). After LPS injection, the mortality rate was higher among Balb/Xid mice, which are B-1 cell deficient, than among wild-type mice (65.0% vs. 0.0%). the Balb/Xid mice also presented a proinflammatory profile of TNF-alpha, IL-6 and nitrite, as well as lower levels of IL-10. in the early phase of LPS stimulation, B-1 cells modulate the macrophage inflammatory response, and the main molecular pathway of that modulation is based on IL-10-mediated intracellular signaling. (C) 2010 Elsevier GmbH. All rights reserved.
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    Caracterização morfológica e funcional de vesículas extracelulares liberadas por células B-1 infectadas por Leishmania (Leishmania) Amazonensis
    (Universidade Federal de São Paulo, 2018-03-26) Toledo, Mayte dos Santos [UNIFESP]; Xander, Patricia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Leishmaniasis is a group of diseases caused by protozoa belonging to the genus Leishmania. The immune response to leishmaniasis is complex and the outcome of the infection depends on several factors, such as genetic composition of Leishmania species and host immunity. Macrophages are known to play a central role in infection by Leishmania parasites and their activation may be influenced by several cell types, such as Th1, Th2, and B-1 lymphocytes. B-1 cells are a subtype of B lymphocytes with peculiar functions in immunity. These cells are able to produce regulatory cytokines (mainly IL-10), natural antibodies and differentiate into phagocytic cells. In addition to cytokines and antibodies, B cells can release different types of extracellular vesicles (EVs) with an important role in intercellular communication, with role in regulating activation and/or modulation of the immune system. However, the production of EVs by B-1 cells and their role in immunity have not yet been demonstrated The aims of this work were to characterize the EVs released by B-1 cells; to study the influence of these EVs on the modulation of lineage macrophages and medullary macrophages from different mouse strains; and to evaluate the role of EVs from B-1 cells in the course of experimental infection by L. (L.) amazonensis. Our results showed that EVs released by B-1 cells infected with the parasite led to a differential activation of J774A.1 macrophages, macrophages from BALB/c and C57BL/6 mice. In addition, EVs released spontaneously by B-1 cells led to a reduction in the lesion progression and parasite burden in BALB/c mice experimentally infected. Thus, this study demonstrated that B-1 cells can release EVs that are capable of altering the functions of macrophages in vitro. In vivo these EVs altered the course of L. (L.) amazonensis infection. This is the first evidence that EVs from B-1 cells can act as a new mechanism of cellular communication between macrophages and B-1 cells.
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    Do chondroitin sulfates with different structures have different activities on chondrocytes and macrophages?
    (Elsevier Science Bv, 2017) da Cunha, Andre L. [UNIFESP]; Aguiar, Jair A. K. [UNIFESP]; Correa da Silva, Flavio S.; Michelacci, Yara M. [UNIFESP]
    The aim of the present study was to investigate the activities of natural chondroitin sulfates (CS) with different structures on cultured chondrocytes and macrophages. CS were isolated from cartilages of bovine trachea (BT), porcine trachea (PT), chicken sternum (Ch) and skate (Sk). The preparations were 90-98% pure, with similar to 1% proteins, nucleic acids and keratan sulfate contaminants. Structural analysis of these CS and of commercial chondroitin 4- and 6-sulfate (C4S, C6S) have shown that most of their disaccharides are monosulfated, with varying proportions of 4- and 6-sulfation, and 2-7% non-sulfated disaccharides. Sk-CS and C6S contained detectable amounts of disulfated disaccharides. All the CS were polydisperse, with modal molecular weights of 26-135 kDa. These CS had anti-inflammatory activities on both chondrocytes and macrophages, but with different efficiencies. On horse and human chondrocytes, they reduced the IL-1 beta-induced liberation of NO and PGE(2), and on RAW 264.7 immortalized macrophage-like cell line, C4S, C6S, Ch and Sk-CS decreased the LPS-induced liberation of TNF-alpha, but did not affect IL-6. In contrast, on bone marrow derived macrophages, C4S, C6S, BT and PT-CS reduced the LPS-induced liberation of TNF-alpha, IL-6, IL-1 beta and NO, indicating that the RAW response to CS was different from that of primary macrophages. (C) 2017 Elsevier B.V. All rights reserved.
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    Downhill exercise-induced changes in gene expression related with macrophage polarization and myogenic cells in the triceps long head of rats
    (Springer, 2015-02-01) Minari, André Luis Araújo [UNIFESP]; Oyama, Lila Missae [UNIFESP]; Santos, Ronaldo Vagner Thomatieli dos [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Macrophages are one of the most heterogenic immune cells involved in skeletal muscle regeneration. After skeletal muscle damage, M1 phenotypes exhibit pro-inflammatory reaction. in a later stage, they are converted to M2 phenotypes with anti-inflammatory properties. To study when gene expressions of macrophage polarization are changed after damage induced by downhill exercise to exhaustion is the objective of this paper. Before (CTRL) and 0 h (G0), 24 h (G24), 48 h (G48) and 72 h (G72) after 18 bouts of downhill exercise, the animals were euthanised, and the triceps were dissected. We measured gene expression of macrophages (CD68 and CD163), myogenic cells (MyoD and myogenin) and quantified cytokine secretion (interleukin (IL)-6, IL-10 and tumour necrosis factor alpha (TNF-alpha)). the CD68 expression was lower in G72 compared with G24 (P = 0.005) while CD163 was higher in G48 compared with G24 (P = 0.04). the MyoD expression was higher in G72 compared with G0 (P = 0.04). the myogenin expression was lower in G24 compared with CTRL (P = 0.01) and restored in G72 compared with G24 (P = 0.007). the TNF-alpha was significantly higher at all times after 24 h (all compared with CTRL, with P = 0.03). the CD68 and CD163 expressions behaved distinctly after exercise, which indicates macrophage polarization between 24 and 48 h. the distinct expression of myogenin, concomitantly with MyoD elevation in G72, indicates that myogenic cell differentiation and the significant change of TNF-alpha level show an important role of this cytokine in these processes.
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    Effect of exercise on glutamine metabolism in macrophages of trained rats
    (Springer, 2009-10-01) Santos, Ronaldo Vagner Thomatieli dos [UNIFESP]; Caperuto, Erico Chagas; Mello, Marco Tulio de [UNIFESP]; Pereira Costa Rosa, Luis Fernando Bicudo; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    This study investigated the effect of exercise on glutamine metabolism in macrophages of trained rats. Rats were divided into three groups: sedentary (SED); moderately trained (MOD) rats that were swim trained 1 h/day, 5 days/week for 6 weeks; and exhaustively trained (EXT) rats that were similarly trained as MOD for 5 weeks and, in the 6th week, trained in three 1-h sessions/day with 150 min of rest between sessions. the animals swam with a load equivalent to 5.5% of their body weight and were killed 1 h after the last exercise session. Cells were collected, and glutamine metabolism in macrophage and function were assayed. Exercise increased phagocytosis in MOD when compared to SED (34.48 +/- 1.79 vs 15.21 +/- 2.91%, P < 0.05); however, H(2)O(2) production was higher in MOD (75.40 +/- 3.48 nmol h x 10(5) cell(-1)) and EXT (79.20 +/- 1.18 nmol h x 10(5) cell(-1)) in relation to SED (32.60 +/- 2.51 nmol h x 10(5) cell(-1), P < 0.05). Glutamine consumption increased in MOD and EXT (26.53 +/- 3.62 and 19.82 +/- 2.62 nmol h x 10(5) cell(-1), respectively) relative to SED (6.72 +/- 0.57 nmol h x 10(5) cell(-1), P < 0.05). Aspartate increased in EXT (9.72 +/- 1.14 nmol h x 10(5) cell(-1)) as compared to SED (1.10 +/- 0.19 nmol h x 10(5) cell(-1), P < 0.05). Glutamine decarboxylation was increased in MOD (12.10 +/- 0.27 nmol h x 10(5) cell(-1)) and EXT (16.40 +/-\ 2.17 nmol h x 10(5) cell(-1)) relative to SED (1.10 +/- 0.06 nmol h x 10(5) cell(-1), P < 0.05). This study suggests an increase in macrophage function post-exercise, which was supported by enhanced glutamine consumption and metabolism, and highlights the importance for glutamine after exercise.
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    Estudo do efeito imunomodulador de vesículas isoladas durante a infecção por trypanosoma cruzi na célula hospedeira
    (Universidade Federal de São Paulo (UNIFESP), 2018-06-28) Andrade, Andre Cronemberger [UNIFESP]; Torrecilhas, Ana Claudia Trocoli [UNIFESP]; http://lattes.cnpq.br/7344293560367809; http://lattes.cnpq.br/7731140733602286
    The extracellular vesicles shed by trypomastigote forms of Trypanosoma cruzi have the ability to interact, increase tissue invasion and modulate the host innate response via TLR2. In T. cruzi infection, induction of the Th1-type response is crucial for promoting protection against the parasite. The aim of the study was to investigate the role of these vesicles as immunomodulatory agents that act during the initial phase of host immune response. THP-1 cells were differentiated into macrophages and infected with T. cruzi. Infected cell culture supernatants of macrophages were collected by ultracentrifugation at different times after infection and the released material was analyzed by NTA. Increased numbers of EVs ranging from 50 to 300 nm were found in the macrophages supernatant 24 hours post infection. Large number of EV from infected compared to non-infected macrophages was observed by scanning electron microscopy. Released EVs contained CD63, CD9, and MHC class II revealing their exosomal and macrophagic origin. No parasite antigens were detected. In addition, the ability of these EVs to translocate NF-kB by TLR2 receptors was evidenced. As a consequence of this interaction, the expression of these receptors is increased. EVs were also able to stimulate the production of proinflammatory cytokines (TNF-α, IL-6 and IL-1β). In this way we observed the potential of EVs derived from T. cruzi infection in the maintenance of the inflammatory response and increase the number of parasites and infected cells in the host.
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    Leishmania enriettii: biochemical characterisation of lipophosphoglycans (LPGs) and glycoinositolphospholipids (GIPLs) and infectivity to Cavia porcellus
    (Biomed Central Ltd, 2015-01-17) Paranaiba, Larissa Ferreira; Assis, Rafael Ramiro de; Nogueira, Paula Monalisa; Torrecilhas, Ana Claudia [UNIFESP]; Campos, Joao Henrique [UNIFESP]; Silveira, Amanda Cardoso de Oliveira; Martins-Filho, Olindo Assis; Pessoa, Natalia Lima; Campos, Marco Antonio; Parreiras, Patricia Martins; Melo, Maria Norma; Gontijo, Nelder de Figueiredo; Soares, Rodrigo Pedro Pinto; Fiocruz MS; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP)
    Background: Leishmania enriettii is a species non-infectious to man, whose reservoir is the guinea pig Cavia porcellus. Many aspects of the parasite-host interaction in this model are unknown, especially those involving parasite surface molecules. While lipophosphoglycans (LPGs) and glycoinositolphospholipids (GIPLs) of Leishmania species from the Old and New World have already been described, glycoconjugates of L. enriettii and their importance are still unknown.Methods: Mice peritoneal macrophages from C57BL/6 and knock-out (TLR2 -/-, TLR4 -/-) were primed with IFN-gamma and stimulated with purified LPG and GIPLs from both species. Nitric oxide and cytokine production were performed. MAPKs (p38 and JNK) and NF-kB activation were evaluated in J774.1 macrophages and CHO cells, respectively.Results: LPGs were extracted, purified and analysed by western-blot, showing that LPG from L88 strain was longer than that of Cobaia strain. LPGs and GIPLs were depolymerised and their sugar content was determined. LPGs from both strains did not present side chains, having the common disaccharide Gal(beta 1,4) Man(alpha 1)-PO4. the GIPL from L88 strain presented galactose in its structure, suggestive of type II GIPL. On the other hand, the GIPL of Cobaia strain presented an abundance of glucose, a characteristic not previously observed. Mice peritoneal macrophages from C57BL/6 and knock-outs (TLR2 -/- and TLR4 -/-) were primed with IFN-gamma and stimulated with glycoconjugates and live parasites. No activation of NO or cytokines was observed with live parasites. On the other hand, LPGs and GIPLs were able to activate the production of NO, IL-6, IL-12 and TNF-alpha preferably via TRL2. However, in CHO cells, only GIPLs were able to activate TRL2 and TRL4. in vivo studies using male guinea pigs (Cavia porcellus) showed that only strain L88 was able to develop more severe ulcerated lesions especially in the presence of salivary gland extract (SGE).Conclusion: the two L. enriettii strains exhibited polymorphisms in their LPGs and GIPLs and those features may be related to a more pro-inflammatory profile in the L88 strain.
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    The macrophage switch in obesity development
    (Pontificia Univ Catolica Sao Paulo, 2016) Castoldi, Angela; de Souza, Cristiane Naffah; Câmara, Niels Olsen Saraiva [UNIFESP]; Moraes-Vieira, Pedro Manoel
    Immune cell infiltration in (white) adipose tissue (AT) during obesity is associated with the development of insulin resistance. In AT, the main population of leukocytes are macrophages. Macrophages can be classified into two major populations: M1, classically activated macrophages, and M2, alternatively activated macrophages, although recent studies have identified a broad range of macrophage subsets. During obesity, AT M1 macrophage numbers increase and correlate with AT inflammation and insulin resistance. Upon activation, pro-inflammatory M1 macrophages induce aerobic glycolysis. By contrast, in lean humans and mice, the number of M2 macrophages predominates. M2 macrophages secrete anti-inflammatory cytokines and utilize oxidative metabolism to maintain AT homeostasis. Here, we review the immunologic and metabolic functions of AT macrophages and their different facets in obesity and the metabolic syndrome.
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    Paracoccidioides brasiliensis GP43-derived peptides are potent modulators of local and systemic inflammatory response
    (Elsevier B.V., 2012-06-01) Konno, Fabiana Toshie de Camargo [UNIFESP]; Maricato, Juliana Terzi [UNIFESP]; Konno, Adriana Yumi de Camargo [UNIFESP]; Guereschi, Marcia Grando [UNIFESP]; Vivanco, Bruno Camolese [UNIFESP]; Feitosa, Luciano dos Santos; Mariano, Mario [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Camilo Castelo Branco
    Paracoccidioidomycosis is a systemic granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis. Its major antigen is a 43 kDa glycoprotein whose peptides embody different functions: P10 peptide, a T-cell epitope, :induces protective response while P4 and P23 peptides inhibit both, macrophage functions and inflammatory reaction, thus facilitating infection. Here we investigated the modulating mechanisms of the immune response exerted by P4 and P23 involved in the latter inhibitory effect on macrophages. Moreover we analyzed the peptides effects in different models in vivo. While evaluating whether P4 and P23 present systemic anti-inflammatory effects in vivo, we showed that their intraperitonial administration decreased footpad swelling in mice infected with either P. brasiliensis or Mycobacterium bovis. Both, qPCR and ELISA assays suggested that this anti-inflammatory effect depended on alterations in the kinetics of production of innate immunity modulators such as TNF-alpha., IL6, IL10 and TLR2. IL10 seems to be early produced than TNF-alpha and IL6, produced later in presence of peptides. Higher doses or intravenously given P4 and P23 resulted in earlier and more prolonged anti-inflammatory effects. Moreover, continuous treatment with P4 and P23 sustained the anti-inflammatory activity throughout. (C) 2012 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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    Peptides from Paracoccidioides brasiliensis GP43 inhibit macrophage functions and inflammatory response
    (Elsevier B.V., 2009-01-01) Konno, Adriana Y. C. [UNIFESP]; Maricato, Juliana Terzi [UNIFESP]; Konno, Fabiana T. C. [UNIFESP]; Mariano, Mario [UNIFESP]; Lopes, Jose Daniel [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Paracoccidioidomycosis (PCM) is a systemic granulomatous disease caused by Paracoccidioides brasiliensis (Pb), a thermal dimorphic fungus. Its major antigen is a 43-kDa glycoprotein. Gp43 embodies different functions: it participates in evasion mechanisms during the installation of primary infection, stimulates granuloma-like formation in vitro and presents T-cell epitopes that induce protective response against the fungus. Here, we investigated epitopes from gp43 inhibitory of both, macrophage functions and inflammatory reaction. Different gp43 peptides, spanning the entire sequence of the molecule, were added to cultures of bone marrow-derived macrophages. After challenge with zymosan or Pb cells, phagocytic indexes were measured. Peptides expressed on the molecule surface were determined by graphic analysis using the Protean module; DNAstar Inc. Two peptides which decreased phagocytic index and were expressed at the surface of the molecule, P4 and P23, were selected for further studies. It was shown that both inhibited the release of NO by zymosan stimulated macrophages while enhanced release of H2O2. the release of TNF-alpha in culture supernatants from in vitro phagocytic tests showed different response depending of P4 concentration (data not shown). in vivo assays with Mycobacterium bovis - bacillus Calmette-Guerin (BCG) or Pb cells demonstrated that these peptides presented non-specific and specific anti-inflammatory properties. (c) 2008 Elsevier Masson SAS. All rights reserved.
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    Uma revisão narrativa sobre a influencia do imunometabolismo na ativação dos inflamassomas em resposta ao toxoplasma gondii
    (Universidade Federal de São Paulo, 2022-12-19) Souza, Rafael Queiroz [UNIFESP]; Bortoluci, Karina Ramalho [UNIFESP]; http://lattes.cnpq.br/0159648961678651; https://lattes.cnpq.br/7588780705511651
    A imunidade inata é a primeira linha de defesa do nosso organismo contra os patógenos e as células dessa imunidade possuem um repertório de receptores restritos a padrões moleculares. Esses receptores são capazes de reconhecer padrões moleculares associados a patógenos e a danos celulares. A família de receptores NLR constituem o maior grupo de receptores citoplasmáticos e podem formar estruturas denominadas inflamassomas. Os inflamassomas são complexos multiproteicos capazes de ativar a caspase-1 e montar uma resposta inflamatória. Um processo muito importante decorrente da ativação da caspase 1 é a morte celular denominada piroptose e a clivagem das citocinas pró inflamatórias IL-1β e IL-18. Já é estabelecido pela literatura que as vias metabólicas e o metabolismo celular são de extrema importância no estudo da imunologia e estão intrinsecamente ligados com as respostas das células do sistema imune. O itaconato é um metabólito importante no contexto inflamatório, com grande efetividade no controle bacteriano , e um dos mecanismos que possibilita essa ação antimicrobiana é a sua ação inibitória sobre a enzima isocitrato liase bacteriana. Outro metabólito de importância no contexto imunológico é o fumarato. Foi observado que o dimetil fumarato (DMF) e o fumarato endógeno são capazes de reagir com a gasdermina D (GSDMD), molécula efetora da piroptose, inibindo esse processo. Um componente celular de grande importância quando falamos de uma resposta imunológica é a mitocôndria, pois desempenha um papel central na regulação de vias de receptores da imunidade inata. O Toxoplasma gondii é um protozoário do filo Apicomplexa que é capaz de subverter o sistema imune inato do hospedeiro pois recruta mitocôndrias do mesmo para o vacúolo parasitóforo. Assim, o objetivo desse trabalho é entender a influência do metabolismo de células imunes na ativação dos inflamassomas durante a infecção pelo T. gondii por meio da revisão de artigos disponíveis em bases dados. Esse entendimento é de grande importância para o campo pois trará embasamento e questões relevantes a serem abordadas em pesquisas futuras.