PMID- 9380718
OWN - NLM
STAT- MEDLINE
DCOM- 19971110
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 94
IP  - 20
DP  - 1997 Sep 30
TI  - Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin 
      basic protein and suppress experimental autoimmune encephalomyelitis.
PG  - 10821-6
AB  - The synthetic amino acid copolymer copolymer 1 (Cop 1) suppresses experimental 
      autoimmune encephalomyelitis (EAE) and is beneficial in multiple sclerosis. To 
      further understand Cop 1 suppressive activity, we studied the cytokine secretion 
      profile of various Cop 1-induced T cell lines and clones. Unlike T cell lines 
      induced by myelin basic protein (MBP), which secreted either T cell helper type 1 
      (Th1) or both Th1 and Th2 cytokines, the T cell lines/clones induced by Cop 1 
      showed a progressively polarized development toward the Th2 pathway, until they 
      completely lost the ability to secrete Th1 cytokines. Our findings indicate that 
      the polarization of the Cop 1-induced lines did not result from the immunization 
      vehicle or the in vitro growing conditions, but rather from the tendency of Cop 1 
      to preferentially induce a Th2 response. The response of all of the Cop 1 
      specific lines/clones, which were originated in the (SJL/JxBALB/c)F1 hybrids, was 
      restricted to the BALB/c parental haplotype. Even though the Cop 1-induced T 
      cells had not been exposed to the autoantigen MBP, they crossreacted with MBP by 
      secretion of interleukin (IL)-4, IL-6, and IL-10. Administration of these T cells 
      in vivo resulted in suppression of EAE induced by whole mouse spinal cord 
      homogenate, in which several autoantigens may be involved. Secretion of 
      anti-inflammatory cytokines by Cop 1-induced suppressor cells, in response to 
      either Cop 1 or MBP, may explain the therapeutic effect of Cop 1 in EAE and in 
      multiple sclerosis.
FAU - Aharoni, R
AU  - Aharoni R
AD  - Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, 
      Israel.
FAU - Teitelbaum, D
AU  - Teitelbaum D
FAU - Sela, M
AU  - Sela M
FAU - Arnon, R
AU  - Arnon R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Interleukin-2)
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Peptides)
RN  - 207137-56-2 (Interleukin-4)
RN  - 5M691HL4BO (Glatiramer Acetate)
SB  - IM
MH  - Adjuvants, Immunologic/*pharmacology
MH  - Animals
MH  - Cell Line
MH  - Cross Reactions
MH  - Encephalomyelitis, Autoimmune, Experimental/immunology/*prevention & control
MH  - Glatiramer Acetate
MH  - Immunosuppressive Agents/*pharmacology
MH  - Interleukin-2/metabolism
MH  - Interleukin-4/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Myelin Basic Protein/*immunology
MH  - Peptides/*pharmacology
MH  - Th2 Cells/*cytology/immunology
PMC - PMC23498
EDAT- 1997/10/06 00:00
MHDA- 1997/10/06 00:01
PMCR- 1998/03/30
CRDT- 1997/10/06 00:00
PHST- 1997/10/06 00:00 [pubmed]
PHST- 1997/10/06 00:01 [medline]
PHST- 1997/10/06 00:00 [entrez]
PHST- 1998/03/30 00:00 [pmc-release]
AID - 2546 [pii]
AID - 10.1073/pnas.94.20.10821 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10821-6. doi: 
      10.1073/pnas.94.20.10821.