Tumor necrosis factor receptor-associated factor 6 mediated the promotion of salivary adenoid cystic carcinoma progression through Smad-p38-JNK signaling pathway induced by TGF-β

2018 ◽  
Vol 47 (6) ◽  
pp. 583-589 ◽  
Author(s):  
Yancan Liang ◽  
Jiuyang Jiao ◽  
Lizhong Liang ◽  
Jin Zhang ◽  
Yingjuan Lu ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Adenoid Cystic Carcinoma ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Jnk Signaling ◽  
Adenoid Cystic ◽  
Jnk Signaling Pathway ◽  
Necrosis Factor

scholarly journals Temporary Blockade of the Tumor Necrosis Factor Receptor Signaling Pathway Impedes the Spread of Scrapie to the Brain

2002 ◽  
Vol 76 (10) ◽  
pp. 5131-5139 ◽  
Author(s):  
Neil A. Mabbott ◽  
Gillian McGovern ◽  
Martin Jeffrey ◽  
Moira E. Bruce
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Transmissible Spongiform Encephalopathies ◽  
Lymphoid Tissues ◽  
Necrosis Factor Alpha ◽  
Spongiform Encephalopathies ◽  
Similar Treatment ◽  
Necrosis Factor

ABSTRACT Although the transmissible spongiform encephalopathies (TSEs) are neurodegenerative diseases, their agents usually replicate and accumulate in lymphoid tissues long before infection spreads to the central nervous system (CNS). Studies of a mouse scrapie model have shown that mature follicular dendritic cells (FDCs), which express the host prion protein (PrPc), are critical for replication of infection in lymphoid tissues. In the absence of mature FDCs, the spread of infection to the CNS is significantly impaired. Tumor necrosis factor alpha (TNF-α) secretion by lymphocytes is important for maintaining FDC networks, and signaling is mediated through TNF receptor 1 (TNFR-1) expressed on FDCs and/or their precursors. A treatment that blocks TNFR signaling leads to the temporary dedifferentiation of mature FDCs, raising the hypothesis that a similar treatment would significantly delay the peripheral pathogenesis of scrapie. Here, specific neutralization of the TNFR signaling pathway was achieved through treatment with a fusion protein consisting of two soluble human TNFR (huTNFR) (p80) domains linked to the Fc portion of human immunoglobulin G1 (huTNFR:Fc). A single treatment of mice with huTNFR:Fc before or shortly after intraperitoneal injection with the ME7 scrapie strain significantly delayed the onset of disease in the CNS and reduced the early accumulation of disease-specific PrP in the spleen. These effects coincided with a temporary dedifferentiation of mature FDCs within 5 days of huTNFR:Fc treatment. We conclude that treatments that specifically inhibit the TNFR signaling pathway may present an opportunity for early intervention in peripherally transmitted TSEs.

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