PMID- 11105778
OWN - NLM
STAT- MEDLINE
DCOM- 20010531
LR  - 20101118
IS  - 0892-3973 (Print)
IS  - 0892-3973 (Linking)
VI  - 22
IP  - 4
DP  - 2000 Nov
TI  - TNF-alpha blockade by a dimeric TNF type I receptor molecule selectively inhibits 
      adaptive immune responses.
PG  - 627-51
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a mediator of severe inflammatory 
      processes, including rheumatoid arthritis. Suppression of TNF with a soluble type 
      I or type II receptor molecule (TNF-RI or TNF-RII) has the potential to decrease 
      cytokine levels and modulate inflammatory diseases in humans. However, it has 
      recently been reported that treatment of mice with a TNF-RI:Fc immunoadhesin 
      protein augmented Gram positive infections and subsequent mortality. To determine 
      if TNF-alpha blockade with soluble TNF-alpha receptors might alter immune system 
      function, assays were assessed in rodents treated with a dimeric form of the p55 
      TNF-RI, Tumor Necrosis Factor-binding protein (TNFbp). Administration of TNFbp 
      resulted in suppression of primary and secondary IgG antibody responses and 
      cell-mediated immune function. No treatment-related differences were detected in 
      immune-enhancing assays or non-specific immune function parameters. Bacterial 
      host resistance assays with Listeria monocytogenes, Staphylococcus aureus or 
      Escherichia coli showed an increase in tissue colony counts only with L. 
      monocytogenes challenged animals following TNFbp administration. These results 
      suggest that TNFbp has the capacity to inhibit adaptive immune function in 
      experimental animal models. Studies suggest that while reducing TNF-alpha is 
      important in controlling cytokine-dependent disease states, maintenance of a 
      threshold level may be critical for normal immune function.
FAU - Colagiovanni, D B
AU  - Colagiovanni DB
AD  - Pharmacology Department, Amgen, Inc, Thousand Oaks, CA 91320, USA.
FAU - Suniga, M A
AU  - Suniga MA
FAU - Frazier, J L
AU  - Frazier JL
FAU - Edwards, C K 3rd
AU  - Edwards CK 3rd
FAU - Fleshner, M
AU  - Fleshner M
FAU - McCay, J A
AU  - McCay JA
FAU - White, K L Jr
AU  - White KL Jr
FAU - Shopp, G M
AU  - Shopp GM
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immunopharmacol Immunotoxicol
JT  - Immunopharmacology and immunotoxicology
JID - 8800150
RN  - 0 (Antigens, CD)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antigens, CD/chemistry/*pharmacology
MH  - Dimerization
MH  - Escherichia coli Infections/immunology
MH  - Female
MH  - Humans
MH  - Immunity/*drug effects
MH  - Immunity, Cellular/drug effects
MH  - Immunoglobulin G/biosynthesis
MH  - Listeriosis/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Inbred DBA
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Tumor Necrosis Factor/chemistry
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Recombinant Proteins/chemistry/pharmacology
MH  - Staphylococcal Infections/immunology
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2000/12/06 11:00
MHDA- 2001/06/02 10:01
CRDT- 2000/12/06 11:00
PHST- 2000/12/06 11:00 [pubmed]
PHST- 2001/06/02 10:01 [medline]
PHST- 2000/12/06 11:00 [entrez]
AID - 10.3109/08923970009016429 [doi]
PST - ppublish
SO  - Immunopharmacol Immunotoxicol. 2000 Nov;22(4):627-51. doi: 
      10.3109/08923970009016429.