Resistance to P. brasiliensis experimental infection of inbred mice is associated with an efficient neutrophil mobilization and activation by mediators of inflammation (2015)
- Authors:
- Sperandio, Felipe Fornias - Universidade Federal de Alfenas (UNIFAL-MG)
- Fernandes, Gisele Pesquero - Universidade Federal do Paraná (UFPR)
- Mendes, Ana Carolina Silvério Cerqueira - Universidade Federal de Alfenas (UNIFAL-MG)
- Bani, Giulia de Alencar Castro - Universidade Federal de Alfenas (UNIFAL-MG)
- Calich, Vera Lucia Garcia
- Burger, Eva - Universidade Federal de Alfenas (UNIFAL-MG)
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- DOI: 10.1155/2015/430525
- Subjects: IMUNOLOGIA; PARACOCCIDIOIDES BRASILIENSIS; INFLAMAÇÃO; NEUTRÓFILOS
- Language: Inglês
- Imprenta:
- Source:
- Título: Mediators of Inflammation
- ISSN: 1466-1861
- Volume/Número/Paginação/Ano: v. 2015, ID 430525, p. 1-10, 2015
- Status:
- Artigo publicado em periódico de acesso aberto (Gold Open Access)
- Versão do Documento:
- Versão publicada (Published version)
- Acessar versão aberta:
-
ABNT
SPERANDIO, Felipe Fornias et al. Resistance to P. brasiliensis experimental infection of inbred mice is associated with an efficient neutrophil mobilization and activation by mediators of inflammation. Mediators of Inflammation, v. 2015, p. 1-10, 2015Tradução . . Disponível em: https://doi.org/10.1155/2015/430525. Acesso em: 16 abr. 2026. -
APA
Sperandio, F. F., Fernandes, G. P., Mendes, A. C. S. C., Bani, G. de A. C., Calich, V. L. G., & Burger, E. (2015). Resistance to P. brasiliensis experimental infection of inbred mice is associated with an efficient neutrophil mobilization and activation by mediators of inflammation. Mediators of Inflammation, 2015, 1-10. doi:10.1155/2015/430525 -
NLM
Sperandio FF, Fernandes GP, Mendes ACSC, Bani G de AC, Calich VLG, Burger E. Resistance to P. brasiliensis experimental infection of inbred mice is associated with an efficient neutrophil mobilization and activation by mediators of inflammation [Internet]. Mediators of Inflammation. 2015 ; 2015 1-10.[citado 2026 abr. 16 ] Available from: https://doi.org/10.1155/2015/430525 -
Vancouver
Sperandio FF, Fernandes GP, Mendes ACSC, Bani G de AC, Calich VLG, Burger E. Resistance to P. brasiliensis experimental infection of inbred mice is associated with an efficient neutrophil mobilization and activation by mediators of inflammation [Internet]. Mediators of Inflammation. 2015 ; 2015 1-10.[citado 2026 abr. 16 ] Available from: https://doi.org/10.1155/2015/430525 - cd28 costimulatory molecule deficiency in more severe paracoccidioides brasiliensis infection but protects mice from life-threatening immunopathology
- Paracoccidioides brasiliensis infection determines dentric cells to diferentiate to the plasmacytoid subpopulation which induces a more severe pulmonary infection when transfered to resistant mice
- The IDO-AhR axis controls Th17/Treg immunity in a pulmonary model of fungal infection
- TLR-2 is a negative regulator of TH17 cells and tissue pathology in a pulmonary model of fungal infection
- Absence of TLR2 results in less severe paracoccidioidomycosis but increased inflammatory response caused by PMN & TH17 cells
- Toll like receptors and the adaptor molecule MYD88 play an important role in pulmonary paracoccidioidomycosis
- TLR2 is a negative regulator of Th17 cells and tissue pathology in a pulmonary model of fungal infection
- Human alfa / beta and gama / delta t cells respond to proteins of the yeast form of paracoccidioides brasiliensis
- The immune response of high (H) and low responders (L) mice (selection III) and F1 (HIII x LIII) hybrids to paracoccidioides brasiliensis infection
- PMN leukocytes play a more prominent role in natural immunity of susceptible than resistant mice to pulmonary paracoccidiodomycosis
Informações sobre a disponibilidade de versões do artigo em acesso aberto coletadas automaticamente via oaDOI API (Unpaywall).
Por se tratar de integração com serviço externo, podem existir diferentes versões do trabalho (como preprints ou postprints), que podem diferir da versão publicada.
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
