PMID- 8872900
OWN - NLM
STAT- MEDLINE
DCOM- 19970110
LR  - 20190116
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 45
IP  - 4
DP  - 1996 Aug 15
TI  - Production of tumor necrosis factor-alpha as a result of glia-T-cell interaction 
      correlates with the pathogenic activity of myelin basic protein-reactive T cells 
      in experimental autoimmune encephalomyelitis.
PG  - 400-9
AB  - Tumor necrosis factor-alpha (TNF-alpha) has attracted the greatest attention as a 
      major factor in experimental autoimmune encephalomyelitis (EAE) pathogenesis. We 
      compared rats undergoing EAE with manipulated but healthy animals by examining 
      TNF-alpha gene expression in cells recovered from the brain. We used reverse 
      transcriptase-polymerase chain reaction (RT-PCR) as a sensitive assay for 
      detection and Northern blot hybridization as a reliable quantitative assay of 
      TNF-alpha mRNA. TNF-alpha gene expression was consistently detected in rats 
      immunized with myelin basic protein (MBP) emulsified in complete Freund adjuvant 
      (CFA), but not in rats immunized with MBP emulsified in incomplete Freund 
      adjuvant (IFA), which does not induce EAE. Similarly, brain-derived cells from 
      rats injected with cloned encephalitogenic T cells contained increased amounts of 
      TNF-alpha mRNA compared with rats injected with nonencephalitogenic T cell clones 
      similar in antigen specificity and in vitro lymphokine-producing capacity. 
      Considering that the differing pathogenic capacity of MBP-reactive T cells might 
      result from differing patterns of interaction with glia, we examined the impact 
      of T-cell-glia interaction in vitro on cytokine gene expression in both cell 
      types. Glial components were efficient in inducing TNF-alpha expression in T 
      cells; T cells and T-cell-derived cytokines could elicit expression of several 
      lymphokine genes in glial cells. Comparison of RT-PCR and blot hybridization 
      assays, however, suggested that cytokine expression was much more efficient, on a 
      per cell basis, in T cells than in glia. TNF-alpha was shown to have direct 
      cytotoxic effect on glial cells, which was greatly enhanced by small amounts of 
      interferon-gamma (IFN-gamma).
FAU - Sun, D
AU  - Sun D
AD  - Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 
      38105, USA.
FAU - Hu, X
AU  - Hu X
FAU - Shah, R
AU  - Shah R
FAU - Zhang, L
AU  - Zhang L
FAU - Coleclough, C
AU  - Coleclough C
LA  - eng
GR  - NS29695/NS/NINDS NIH HHS/United States
GR  - P30CA21765/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Cell Communication/immunology
MH  - Cell Line/chemistry/immunology
MH  - Cell Survival/drug effects/immunology
MH  - Central Nervous System/cytology
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology
MH  - Gene Expression Regulation/immunology
MH  - Guinea Pigs
MH  - Interferon-gamma/pharmacology
MH  - Myelin Basic Protein/analysis
MH  - Neuroglia/cytology/drug effects/*immunology
MH  - Rats
MH  - Rats, Inbred Lew
MH  - T-Lymphocytes/chemistry/cytology/*immunology
MH  - Tumor Necrosis Factor-alpha/*genetics/pharmacology
EDAT- 1996/08/15 00:00
MHDA- 2000/06/20 09:00
CRDT- 1996/08/15 00:00
PHST- 1996/08/15 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1996/08/15 00:00 [entrez]
AID - 10.1002/(SICI)1097-4547(19960815)45:4<400::AID-JNR9>3.0.CO;2-D [pii]
AID - 10.1002/(SICI)1097-4547(19960815)45:4<400::AID-JNR9>3.0.CO;2-D [doi]
PST - ppublish
SO  - J Neurosci Res. 1996 Aug 15;45(4):400-9. doi: 
      10.1002/(SICI)1097-4547(19960815)45:4<400::AID-JNR9>3.0.CO;2-D.