PMID- 10650887
OWN - NLM
STAT- MEDLINE
DCOM- 20000217
LR  - 20191103
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 59
IP  - 2
DP  - 2000 Jan 15
TI  - Passive transfer of experimental autoimmune encephalomyelitis in Wistar rats:
      dissociation of clinical symptoms and biochemical alterations.
PG  - 283-90
AB  - We have used passive transfer of myelin-reactive lymphocytes in the Wistar rat
      model of experimental autoimmune encephalomyelitis (EAE) to investigate the
      nature of the central nervous system immunopathological alterations induced by
      these cells. Mononuclear cells from lymph nodes or spleen from sick
      myelin/complete Freund's adjuvant-immunized donors did not transfer clinical
      disease. However, depending on the previous treatment of the transferred cells,
      recipients develop central nervous system biochemical and histological
      alterations. Fresh cells from lymph nodes immediately transferred after
      procurement from the sick EAE donor rat were capable of inducing the most
      significant diminution in the content of myelin basic protein, sulfatides, and
      2',3'-cyclic nucleotide-3'-phosphohydrolase activity, with concomitant
      inflammatory infiltrations of white matter, principally in spinal cord and
      cerebellar lobules. Similar alterations were observed when animals were injected 
      with spleen mononuclear cells activated in the presence of a nonspecific mitogen 
      as concanavalin A. However, antigen-specific activated spleen cells generated by 
      culturing in the presence of bovine myelin induced alterations to a lesser
      degree. Results point to a dissociation of the clinical disease from the central 
      nervous system biochemical and histopathological lesions occurring in the
      EAE-transferred Wistar rats and indicate that these alterations in EAE are
      induced principally by T cells activated in vivo rather than by cells activated
      in vitro by myelin antigens. Therefore, these findings suggest a possible
      participation of lymphocytes unlike the encephalitogenic T cells in the induction
      of the described alterations and provide a useful model to explore further the
      subclinical responses to this experimental disease.
FAU - Degano, A L
AU  - Degano AL
AD  - Centro de Investigaciones en Quimica Bioliogica de Cordoba (CIQUIBIC),
      UNC-CONICET, Departamento de Quimica Biologica, Facultad de Ciencias Quimicas,
      Universidad Nacional de Cordoba, Argentina.
FAU - Roth, G A
AU  - Roth GA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Autoantibodies)
RN  - 0 (Myelin Basic Protein)
RN  - 11028-71-0 (Concanavalin A)
RN  - EC 3.1.4.- (2',3'-Cyclic-Nucleotide Phosphodiesterases)
SB  - IM
MH  - 2',3'-Cyclic-Nucleotide Phosphodiesterases/analysis
MH  - Animals
MH  - Autoantibodies/blood
MH  - Cattle
MH  - Cells, Cultured
MH  - Central Nervous System/*chemistry/immunology
MH  - Concanavalin A
MH  - Encephalomyelitis, Autoimmune,
      Experimental/*immunology/metabolism/physiopathology
MH  - Female
MH  - Male
MH  - Myelin Basic Protein/*immunology/pharmacology
MH  - Myelin Sheath/enzymology/immunology
MH  - Rats
MH  - Rats, Wistar
MH  - T-Lymphocytes/cytology/enzymology/*transplantation
EDAT- 2000/01/29 09:00
MHDA- 2000/02/19 09:00
CRDT- 2000/01/29 09:00
PHST- 2000/01/29 09:00 [pubmed]
PHST- 2000/02/19 09:00 [medline]
PHST- 2000/01/29 09:00 [entrez]
AID - 10.1002/(SICI)1097-4547(20000115)59:2<283::AID-JNR15>3.0.CO;2-S [pii]
AID - 10.1002/(sici)1097-4547(20000115)59:2<283::aid-jnr15>3.0.co;2-s [doi]
PST - ppublish
SO  - J Neurosci Res. 2000 Jan 15;59(2):283-90. doi:
      10.1002/(sici)1097-4547(20000115)59:2<283::aid-jnr15>3.0.co;2-s.