Protective role of NKT cells and macrophage M2-drivenphenotype in bleomycin-induced pulmonary fibrosis (2018)
- Authors:
- USP affiliated authors: CÂMARA, NIELS OLSEN SARAIVA - RUSP ; HIYANE, MEIRE IOSHIE - ICB
- Unidades: RUSP; ICB
- DOI: 10.1007/s10787-017-0383-7
- Subjects: INFLAMAÇÃO; FENÓTIPOS; INTERLEUCINA; FIBROSE PULMONAR; MACROFAGOS; INTERFERON
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Inflammopharmacology
- ISSN: 1568-5608
- Volume/Número/Paginação/Ano: v. 26, p. 491-504, 2018
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
GRABARZ, Felip et al. Protective role of NKT cells and macrophage M2-drivenphenotype in bleomycin-induced pulmonary fibrosis. Inflammopharmacology, v. 26, p. 491-504, 2018Tradução . . Disponível em: https://doi.org/10.1007/s10787-017-0383-7. Acesso em: 24 fev. 2026. -
APA
Grabarz, F., Aguiar, C. F., Correa-Costa, M., Hyane, M. I., Andrade-Oliveira, V., Landgraf, M. A., & Câmara, N. O. S. (2018). Protective role of NKT cells and macrophage M2-drivenphenotype in bleomycin-induced pulmonary fibrosis. Inflammopharmacology, 26, 491-504. doi:10.1007/s10787-017-0383-7 -
NLM
Grabarz F, Aguiar CF, Correa-Costa M, Hyane MI, Andrade-Oliveira V, Landgraf MA, Câmara NOS. Protective role of NKT cells and macrophage M2-drivenphenotype in bleomycin-induced pulmonary fibrosis [Internet]. Inflammopharmacology. 2018 ; 26 491-504.[citado 2026 fev. 24 ] Available from: https://doi.org/10.1007/s10787-017-0383-7 -
Vancouver
Grabarz F, Aguiar CF, Correa-Costa M, Hyane MI, Andrade-Oliveira V, Landgraf MA, Câmara NOS. Protective role of NKT cells and macrophage M2-drivenphenotype in bleomycin-induced pulmonary fibrosis [Internet]. Inflammopharmacology. 2018 ; 26 491-504.[citado 2026 fev. 24 ] Available from: https://doi.org/10.1007/s10787-017-0383-7 - Immune regulatory properties of allogeneic adipose-derived mesenchymal stem cells in the treatment of experimental autoimmune diabetes
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Informações sobre o DOI: 10.1007/s10787-017-0383-7 (Fonte: oaDOI API)
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