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Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis.
Proc Natl Acad Sci U S A 1997; 94(20):10821-6PN

Abstract

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.

Authors+Show Affiliations

Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9380718

Citation

Aharoni, R, et al. "Copolymer 1 Induces T Cells of the T Helper Type 2 That Crossreact With Myelin Basic Protein and Suppress Experimental Autoimmune Encephalomyelitis." Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 20, 1997, pp. 10821-6.
Aharoni R, Teitelbaum D, Sela M, et al. Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis. Proc Natl Acad Sci USA. 1997;94(20):10821-6.
Aharoni, R., Teitelbaum, D., Sela, M., & Arnon, R. (1997). Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis. Proceedings of the National Academy of Sciences of the United States of America, 94(20), pp. 10821-6.
Aharoni R, et al. Copolymer 1 Induces T Cells of the T Helper Type 2 That Crossreact With Myelin Basic Protein and Suppress Experimental Autoimmune Encephalomyelitis. Proc Natl Acad Sci USA. 1997 Sep 30;94(20):10821-6. PubMed PMID: 9380718.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Copolymer 1 induces T cells of the T helper type 2 that crossreact with myelin basic protein and suppress experimental autoimmune encephalomyelitis. AU - Aharoni,R, AU - Teitelbaum,D, AU - Sela,M, AU - Arnon,R, PY - 1997/10/6/pubmed PY - 1997/10/6/medline PY - 1997/10/6/entrez SP - 10821 EP - 6 JF - Proceedings of the National Academy of Sciences of the United States of America JO - Proc. Natl. Acad. Sci. U.S.A. VL - 94 IS - 20 N2 - 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. SN - 0027-8424 UR - https://www.unboundmedicine.com/medline/citation/9380718/Copolymer_1_induces_T_cells_of_the_T_helper_type_2_that_crossreact_with_myelin_basic_protein_and_suppress_experimental_autoimmune_encephalomyelitis_ L2 - http://www.pnas.org/cgi/pmidlookup?view=long&pmid=9380718 DB - PRIME DP - Unbound Medicine ER -