PMID- 9780152
OWN - NLM
STAT- MEDLINE
DCOM- 19981104
LR  - 20061115
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 161
IP  - 8
DP  - 1998 Oct 15
TI  - Long-lasting protective immunity to experimental autoimmune encephalomyelitis 
      following vaccination with naked DNA encoding C-C chemokines.
PG  - 3870-9
AB  - DNA vaccination represents a novel means of expressing Ag in vivo for the 
      generation of both humoral and cellular immune responses. The current study uses 
      this technology to elicit protective immunity against experimental autoimmune 
      encephalomyelitis (EAE), a T cell-mediated autoimmune disease of the central 
      nervous system that serves as an experimental model for multiple sclerosis. 
      RT-PCR verified by Southern blotting and sequencing of PCR products of four 
      different C-C chemokines, macrophage-inflammatory protein-1alpha (MIP-1alpha), 
      monocyte-chemotactic protein-1 (MCP-1), MIP-1beta, and RANTES, were performed on 
      brain samples from EAE rats to evaluate mRNA transcription at different stages of 
      disease. Each PCR product was then used as a construct for naked DNA vaccination. 
      The subsequent in vivo immune response to MIP-1alpha or MCP-1 DNA vaccines 
      prevented EAE, even if disease was induced 2 mo after administration of naked DNA 
      vaccines. In contrast, administration of the MIP-1beta naked DNA significantly 
      aggravated the disease. Generation of in vivo immune response to RANTES naked DNA 
      had no notable effect on EAE. MIP-1alpha, MCP-1, and MIP-1beta mRNA transcription 
      in EAE brains peaked at the onset of disease and declined during its remission, 
      whereas RANTES transcription increased in EAE brains only following recovery. 
      Immunization of CFA without the encephalitogenic epitope did not elicit the 
      anti-C-C chemokine regulatory response in DNA-vaccinated rats. Thus, modulation 
      of EAE with C-C chemokine DNA vaccines is dependent on targeting chemokines that 
      are highly transcribed at the site of inflammation at the onset of disease.
FAU - Youssef, S
AU  - Youssef S
AD  - Department of Immunology, Bruce Rappaport Faculty of Medicine, Technion, Haifa, 
      Israel.
FAU - Wildbaum, G
AU  - Wildbaum G
FAU - Maor, G
AU  - Maor G
FAU - Lanir, N
AU  - Lanir N
FAU - Gour-Lavie, A
AU  - Gour-Lavie A
FAU - Grabie, N
AU  - Grabie N
FAU - Karin, N
AU  - Karin N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokines, CC)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vaccines, DNA)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Chemokines, CC/genetics/*immunology
MH  - DNA/administration & dosage/immunology
MH  - Encephalomyelitis, Autoimmune, Experimental/immunology/*prevention & control
MH  - Female
MH  - Molecular Sequence Data
MH  - RNA, Messenger/immunology
MH  - Rats
MH  - Rats, Inbred Lew
MH  - *Vaccination
MH  - Vaccines, DNA/administration & dosage/*immunology
EDAT- 1998/10/21 00:00
MHDA- 1998/10/21 00:01
CRDT- 1998/10/21 00:00
PHST- 1998/10/21 00:00 [pubmed]
PHST- 1998/10/21 00:01 [medline]
PHST- 1998/10/21 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1998 Oct 15;161(8):3870-9.