Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences (2010)
- Authors:
- Trombone, A. P. - Universidade de São Paulo (USP)
- Claudino, M.
- Colavite, P.
- Assis, Gérson Francisco de
- Ávila-Campos, Mario Julio - Universidade de São Paulo (USP)
- Silva, João Santana da
- Campanelli, Ana Paula
- Ibañez, O. M. - Instituto Butantan (IB)
- De Franco, M. - Instituto Butantan (IB)
- Garlet, Gustavo Pompermaier
- USP affiliated authors: ASSIS, GERSON FRANCISCO DE - FOB ; CAMPANELLI, ANA PAULA - FOB ; GARLET, GUSTAVO POMPERMAIER - FOB ; SILVA, JOÃO SANTANA DA - FMRP ; CAMPOS, MARIO JULIO AVILA - ICB
- Unidades: FOB; FMRP; ICB
- DOI: 10.1038/gene.2010.13
- Subjects: PERIODONTITE; ARTRITE REUMATOIDE; INFLAMAÇÃO; CITOCINAS
- Language: Inglês
- Imprenta:
- Publisher place: Basingstoke
- Date published: 2010
- Source:
- Título: Genes and Immunity
- ISSN: 1466-4879
- Volume/Número/Paginação/Ano: v. 11, n. 6, p. 479-489, Sept. 2010
- Status:
- Artigo possui versão em acesso aberto em repositório (Green Open Access)
- Versão do Documento:
- Versão submetida (Pré-print)
- Acessar versão aberta:
-
ABNT
TROMBONE, A. P. et al. Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences. Genes and Immunity, v. 11, n. 6, p. 479-489, 2010Tradução . . Disponível em: https://doi.org/10.1038/gene.2010.13. Acesso em: 01 abr. 2026. -
APA
Trombone, A. P., Claudino, M., Colavite, P., Assis, G. F. de, Ávila-Campos, M. J., Silva, J. S. da, et al. (2010). Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences. Genes and Immunity, 11( 6), 479-489. doi:10.1038/gene.2010.13 -
NLM
Trombone AP, Claudino M, Colavite P, Assis GF de, Ávila-Campos MJ, Silva JS da, Campanelli AP, Ibañez OM, De Franco M, Garlet GP. Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences [Internet]. Genes and Immunity. 2010 ; 11( 6): 479-489.[citado 2026 abr. 01 ] Available from: https://doi.org/10.1038/gene.2010.13 -
Vancouver
Trombone AP, Claudino M, Colavite P, Assis GF de, Ávila-Campos MJ, Silva JS da, Campanelli AP, Ibañez OM, De Franco M, Garlet GP. Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences [Internet]. Genes and Immunity. 2010 ; 11( 6): 479-489.[citado 2026 abr. 01 ] Available from: https://doi.org/10.1038/gene.2010.13 - Regulatory T cells attenuate experimental periodontitis progression in mice
- TNF-alpha/CCL3-5/CCR5 cascade mediates RANKL plus cells migration in inflammatory bone resorption
- Functional interferences in host inflammatory immune response by airway allergic inflammation restrain experimental periodontitis development in mice
- Association of human T lymphotropic virus 1 amplification of periodontitis severity with altered cytokine expression in response to a standard periodontopathogen infection
- Evidences of the cooperative role of the chemokines CCL3, CCL4 and CCL5 and its receptors CCR1+ and CCR5+ in RANKL+ cell migration throughout experimental periodontitis in mice
- The cooperative role of CCR1 and CCR5 in the migration of osteoclast precursors and RANKL+ Cells throughout inflammatory bone loss after periodontal infection
- Tumor necrosis factor-alpha -308G/A single nucleotide polymorphism and red-complex periodontopathogens are independently associated with increased levels of tumor necrosis factor-alpha in diseased periodontal tissues
- Experimental periodontitis in mice selected for maximal or minimal inflammatory reactions: increased inflammatory immune responsiveness drives increased alveolar bone loss without enhancing the control of periodontal infection
- Shared genetic susceptibility and functional interferences in the interaction between periodontitis and arthritis: a possible role for NRAMP1/SLC11A1
- The role of MIP-1A (CCL3) on the immunomodulation of experimental periodontal disease in mice
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