scholarly journals Monoclonal antibody against interferon gamma can prevent experimental cerebral malaria and its associated overproduction of tumor necrosis factor.

1989 ◽  
Vol 86 (14) ◽  
pp. 5572-5574 ◽  
Author(s):  
G. E. Grau ◽  
H. Heremans ◽  
P. F. Piguet ◽  
P. Pointaire ◽  
P. H. Lambert ◽  
...  
1996 ◽  
Vol 174 (5) ◽  
pp. 1091-1097 ◽  
Author(s):  
M. B. van Hensbroek ◽  
A. Palmer ◽  
E. Onyiorah ◽  
G. Schneider ◽  
S. Jaffar ◽  
...  

2002 ◽  
Vol 70 (10) ◽  
pp. 5857-5859 ◽  
Author(s):  
Benjamin Stoelcker ◽  
Thomas Hehlgans ◽  
Karin Weigl ◽  
Horst Bluethmann ◽  
Georges E. Grau ◽  
...  

ABSTRACT Using tumor necrosis factor receptor type 2 (TNFR2)-deficient mice and generating bone marrow chimeras which express TNFR2 on either hematopoietic or nonhematopoietic cells, we demonstrated the requirement for TNFR2 expression on tissue cells to induce lethal cerebral malaria. Thus, TNFR2 on the brain vasculature mediates tumor necrosis factor-induced neurovascular lesions in experimental cerebral malaria.


1997 ◽  
Vol 27 (7) ◽  
pp. 1719-1725 ◽  
Author(s):  
Rudolf Lucas ◽  
Pierre Juillard ◽  
Els Decoster ◽  
Mireille Redard ◽  
Danielle Burger ◽  
...  

1999 ◽  
Vol 43 (5) ◽  
pp. 1027-1033 ◽  
Author(s):  
Nancy S. Postma ◽  
Rob C. Hermsen ◽  
Daan J. A. Crommelin ◽  
Wijnand M. C. Eling ◽  
Jan Zuidema

ABSTRACT The introduction of reactive thiol groups in recombinant human tumor necrosis factor (TNF) alpha (rhTNF-α) by the reagent succinimidyl-S-acetylthioacetate resulted in the formation of a chemically stabilized rhTNF-α trimer (rhTNFα-AT; as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis). rhTNFα-AT showed a substantially enhanced protective efficacy against the development of experimental murine cerebral malaria (ECM) after intravenous injection compared to the protective efficacy of nonmodified rhTNF-α. Administration of thiolated rhTNF-α with protected thiol groups (rhTNFα-ATA; no stabilized trimers in vitro) exhibited the same protective efficacy against ECM, while in vitro bioactivity was reduced. Parasitemia was significantly suppressed in rhTNF-treated mice that were protected against ECM but not in treated mice that developed ECM. Protection against ECM was not related to increased concentrations in plasma of soluble TNF receptor 1 and 2 directly after injection or at the moment of development of ECM in nontreated mice. The results indicate that thiolation of rhTNF-α leads to the formation of stable trimers with increased potential in vivo.


Hybridoma ◽  
1994 ◽  
Vol 13 (3) ◽  
pp. 183-190 ◽  
Author(s):  
PHILIP R. TEMPEST ◽  
ELENA BARBANTI ◽  
PATRICIA BREMNER ◽  
FRANK J. CARR ◽  
MARTA GHISLIERI ◽  
...  

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