Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells (2018)
- Authors:
- USP affiliated authors: CUNHA, THIAGO MATTAR - FMRP ; ALVES FILHO, JOSÉ CARLOS FARIAS - FMRP ; LOUZADA JÚNIOR, PAULO - FMRP ; CUNHA, FERNANDO DE QUEIROZ - FMRP
- Unidade: FMRP
- DOI: 10.1186/s13075-018-1609-9
- Subjects: ARTRITE REUMATOIDE; FUMANTES; INFLAMAÇÃO; HIDROCARBONETOS
- Keywords: Rheumatoid arthritis; Cigarette smoke; Inflammation; Polycyclic aromatic hydrocarbons; Th17
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Arthritis Research & Therapy
- ISSN: 1478-6362
- Volume/Número/Paginação/Ano: v.20, n.1, art. 119, 2018
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by-nc-nd
-
ABNT
TALBOT, Jhimmy et al. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells. Arthritis Research & Therapy, v. 20, n. 1, 2018Tradução . . Disponível em: https://doi.org/10.1186/s13075-018-1609-9. Acesso em: 27 dez. 2025. -
APA
Talbot, J., Peres, R. S., Pinto, L. G., Oliveira, R. D. R., Lima, K. A., Donate, P. B., et al. (2018). Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells. Arthritis Research & Therapy, 20( 1). doi:10.1186/s13075-018-1609-9 -
NLM
Talbot J, Peres RS, Pinto LG, Oliveira RDR, Lima KA, Donate PB, Silva JR, Ryffel B, Cunha TM, Alves Filho JCF, Liew FY, Louzada Júnior P, Cunha F de Q. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells [Internet]. Arthritis Research & Therapy. 2018 ;20( 1):[citado 2025 dez. 27 ] Available from: https://doi.org/10.1186/s13075-018-1609-9 -
Vancouver
Talbot J, Peres RS, Pinto LG, Oliveira RDR, Lima KA, Donate PB, Silva JR, Ryffel B, Cunha TM, Alves Filho JCF, Liew FY, Louzada Júnior P, Cunha F de Q. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells [Internet]. Arthritis Research & Therapy. 2018 ;20( 1):[citado 2025 dez. 27 ] Available from: https://doi.org/10.1186/s13075-018-1609-9 - Toll-like receptor 9 activation in neutrophils impairs chemotaxis and reduces sepsis outcome
- Superoxide anion-induced pain and inflammation depends on TNFα/TNFR1 signaling in mice
- The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β
- Trans-chalcone attenuates pain and inflammation in experimental acute gout arthritis in mice
- Hesperidin methylchalcone suppresses experimental gout arthritis in mice by inhibiting NF-KB activation
- Differential regulation of oxidative stress and cytokine production by endothelin ETA and ETB receptors in superoxide anion-induced inflammation and pain in mice
- Bosentan, a mixed endothelin receptor antagonist, inhibits superoxide anion-induced pain and inflammation in mice
- Curcumin inhibits superoxide anion-induced pain-like behavior and leukocyte recruitment by increasing Nrf2 expression and reducing NF-kB activation
- 15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice
- The PI3Kγ/AKT signaling pathway mediates peripheral antinociceptive action of dipyrone
Informações sobre o DOI: 10.1186/s13075-018-1609-9 (Fonte: oaDOI API)
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
