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Evaluation the mechanisms involved in the survival of long-lived antibody-secreting cells induced by IL-17- released from neutrophil extracellular traps

Grant number: 15/12224-6
Support Opportunities:Scholarships abroad - Research
Effective date (Start): September 01, 2016
Effective date (End): November 30, 2016
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:Carla Lima da Silva
Grantee:Carla Lima da Silva
Host Investigator: Bernhard Ryffel
Host Institution: Instituto Butantan. Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Research place: Université d'Orléans, France  
Associated research grant:13/07467-1 - CeTICS - Center of Toxins, Immune-Response and Cell Signaling, AP.CEPID


Results from our research group have shown that the memory response induced by T. nattereri venom in Balb/c mice is characterized by a chronic inflammation containing IL-17A-producing neutrophils. Moreover, we identified IL-17A retained in neutrophil extracellular traps (NET) in peritoneal inflamed cavity and spleen. Using the antagonist antibody of the IL-1 receptor (IL-1Ra) or blocking the enzymatic activity of COX-2 with Celecoxib treatment we showed that IL-17A-producing neutrophils are dependent on IL-1² and COX-2, but independent on T cells response (using CD4 KO mice). We confirmed that the survival of ASC B220neg in chronic inflamed peritoneal cavity is positive regulated by the neutrophilic inflammation and by IL-1 and COX-2 activities. Also, the ASC B220neg survival was negative regulated by T cells, Rag1 or CD28. Given the important role of IL-1 in promoting IL-17 production by neutrophils (Coccia et al., 2012), the inflamasome control of IL-1 production (Bank & Ansorge, 2001), the positive regulation of ASC B220neg survival by IL-17 in in vivo (Grund et al., 2012) and in vitro models (Grund et al., 2013), and the essential role of IL-17A-producing neutrophils on ASC B220neg survival it would be expected the subsequently that, IL-17 on NET exerts control over survival of terminal differentiated ASC. This hypothesis lead us to propose the investigation of the innate signals as inflamasome complex driven IL-17 production by neutrophils, NET extrusion and IL-17 externalization on NET involved in the maintenance of ASC survival. We speculate that IL-17 present in the NETs may have additional effects on ASC survival. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
DOS SANTOS, JANAINA CARDOSO; GRUND, LIDIANE ZITO; SEIBERT, CARLA SIMONE; MARQUES, ELINEIDE EUGENIO; SOARES, ANDERSON BRITO; QUESNIAUX, VALERIE F.; RYFFEL, BERNHARD; LOPES-FERREIRA, MONICA; LIMA, CARLA. Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury. SCIENTIFIC REPORTS, v. 7, . (13/07467-1, 15/12224-6, 15/12225-2)

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