Assessing multiple sclerosis activity: is the in vitro production of tumor necrosis factor-α, interleukins 2, 6, 4, and 10, and immunoglobulin G of value?

1999 ◽  
Vol 246 (11) ◽  
pp. 1041-1050 ◽  
Author(s):  
M. Schluep ◽  
Guy van Melle ◽  
Hugues Henry ◽  
Claudio Städler ◽  
Béatrice Roth-Wicky ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Tumor Necrosis Factor ◽  
Immunoglobulin G ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
In Vitro Production ◽  
Factor Α ◽  
Vitro Production ◽  
Necrosis Factor

Pneumocystis carinii stimulates in vitro production of tumor necrosis factor-α by human macrophages

1991 ◽  
Vol 180 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Enrica Tamburrini ◽  
Andrea De Luca ◽  
Giulio Ventura ◽  
Giuseppe Maiuro ◽  
Alessandra Siracusano ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Pneumocystis Carinii ◽  
In Vitro Production ◽  
Human Macrophages ◽  
Factor Α ◽  
Vitro Production ◽  
Necrosis Factor

scholarly journals In Vivo and in Vitro Evidence for the Involvement of Tumor Necrosis Factor-α in the Induction of Leptin by Lipopolysaccharide*

Endocrinology ◽  
1998 ◽  
Vol 139 (5) ◽  
pp. 2278-2283 ◽  
Author(s):  
Brian N. Finck ◽  
Keith W. Kelley ◽  
Robert Dantzer ◽  
Rodney W. Johnson
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Ectopic HOXB4 overcomes the inhibitory effect of tumor necrosis factor-α on Fanconi anemia hematopoietic stem and progenitor cells

Blood ◽  
2009 ◽  
Vol 113 (21) ◽  
pp. 5111-5120 ◽  
Author(s):  
Michael D. Milsom ◽  
Bernhard Schiedlmeier ◽  
Jeff Bailey ◽  
Mi-Ok Kim ◽  
Dandan Li ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Fanconi Anemia ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ectopic Expression ◽  
Hematopoietic Stem ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

AbstractEctopic delivery of HOXB4 elicits the expansion of engrafting hematopoietic stem cells (HSCs). We hypothesized that inhibition of tumor necrosis factor-α (TNF-α) signaling may be central to the self-renewal signature of HOXB4. Because HSCs derived from Fanconi anemia (FA) knockout mice are hypersensitive to TNF-α, we studied Fancc−/− HSCs to determine the physiologic effects of HOXB4 on TNF-α sensitivity and the relationship of these effects to the engraftment defect of FA HSCs. Overexpression of HOXB4 reversed the in vitro hypersensitivity to TNF-α of Fancc−/− HSCs and progenitors (P) and partially rescued the engraftment defect of these cells. Coexpression of HOXB4 and the correcting FA-C protein resulted in full correction compared with wild-type (WT) HSCs. Ectopic expression of HOXB4 resulted in a reduction in both apoptosis and reactive oxygen species in Fancc−/− but not WT HSC/P. HOXB4 overexpression was also associated with a significant reduction in surface expression of TNF-α receptors on Fancc−/− HSC/P. Finally, enhanced engraftment was seen even when HOXB4 was expressed in a time-limited fashion during in vivo reconstitution. Thus, the HOXB4 engraftment signature may be related to its effects on TNF-α signaling, and this pathway may be a molecular target for timed pharmacologic manipulation of HSC during reconstitution.

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