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Monoclonal Antibody against T-Cell Receptor alphabeta Induces Self-Tolerance in Chronic Experimental Autoimmune Encephalomyelitis.

Lavasani, Shahram LU ; Dzhambazov, Balik LU and Andersson, M (2007) In Scandinavian Journal of Immunology 65(1). p.39-47
Abstract
The therapeutic effect of monoclonal antibody (H57-597 MoAb) against T-cell receptor (TCR) alpha beta has been investigated on MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE), as a model system for T-cell-mediated chronic inflammation in the central nervous system (CNS). Short-term administration of the anti-TCR alpha beta immediately after immunization protected the mice from EAE. Furthermore, anti-TCR alpha beta treatment on an established disease restored the self-tolerance which led to a complete remission of EAE and a dramatic reduction of inflammatory cells in the CNS, while treatment with control antibody (hamster IgG) was ineffective. The remission was durable and not associated with disappearance of autoreactive... (More)
The therapeutic effect of monoclonal antibody (H57-597 MoAb) against T-cell receptor (TCR) alpha beta has been investigated on MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE), as a model system for T-cell-mediated chronic inflammation in the central nervous system (CNS). Short-term administration of the anti-TCR alpha beta immediately after immunization protected the mice from EAE. Furthermore, anti-TCR alpha beta treatment on an established disease restored the self-tolerance which led to a complete remission of EAE and a dramatic reduction of inflammatory cells in the CNS, while treatment with control antibody (hamster IgG) was ineffective. The remission was durable and not associated with disappearance of autoreactive T cells as measured by persistence of MOG-reactive T-cell proliferation in vitro. However, MOG-reactive T cells from anti-TCR-treated animals produced significantly lower amounts of inflammatory TNF-alpha and IFN-gamma. In addition, while a transient deletion of CD4(+) and CD8(+) T cells was observed, a population of T cells expressing CD3, NK1.1 and CD69 (NKT cells) were expanding. By transfer of spleen cells from anti-TCR MoAb-treated animals, we could show that the tolerogenic capacity can be transferred to untreated recipients with EAE. The data indicate therapeutic effect of anti-TCR alpha beta MoAb (H57-597), which represents a promising approach in treatment of T-cell-mediated autoimmune diseases. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Scandinavian Journal of Immunology
volume
65
issue
1
pages
39 - 47
publisher
Wiley-Blackwell
external identifiers
  • wos:000242907200006
  • scopus:33845713001
ISSN
1365-3083
DOI
10.1111/j.1365-3083.2006.01866.x
language
English
LU publication?
yes
id
610f8db3-ff65-4090-8985-9f77dc2dd1c5 (old id 165048)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17212765&dopt=Abstract
date added to LUP
2007-07-30 16:14:46
date last changed
2017-10-22 04:37:31
@article{610f8db3-ff65-4090-8985-9f77dc2dd1c5,
  abstract     = {The therapeutic effect of monoclonal antibody (H57-597 MoAb) against T-cell receptor (TCR) alpha beta has been investigated on MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE), as a model system for T-cell-mediated chronic inflammation in the central nervous system (CNS). Short-term administration of the anti-TCR alpha beta immediately after immunization protected the mice from EAE. Furthermore, anti-TCR alpha beta treatment on an established disease restored the self-tolerance which led to a complete remission of EAE and a dramatic reduction of inflammatory cells in the CNS, while treatment with control antibody (hamster IgG) was ineffective. The remission was durable and not associated with disappearance of autoreactive T cells as measured by persistence of MOG-reactive T-cell proliferation in vitro. However, MOG-reactive T cells from anti-TCR-treated animals produced significantly lower amounts of inflammatory TNF-alpha and IFN-gamma. In addition, while a transient deletion of CD4(+) and CD8(+) T cells was observed, a population of T cells expressing CD3, NK1.1 and CD69 (NKT cells) were expanding. By transfer of spleen cells from anti-TCR MoAb-treated animals, we could show that the tolerogenic capacity can be transferred to untreated recipients with EAE. The data indicate therapeutic effect of anti-TCR alpha beta MoAb (H57-597), which represents a promising approach in treatment of T-cell-mediated autoimmune diseases.},
  author       = {Lavasani, Shahram and Dzhambazov, Balik and Andersson, M},
  issn         = {1365-3083},
  language     = {eng},
  number       = {1},
  pages        = {39--47},
  publisher    = {Wiley-Blackwell},
  series       = {Scandinavian Journal of Immunology},
  title        = {Monoclonal Antibody against T-Cell Receptor alphabeta Induces Self-Tolerance in Chronic Experimental Autoimmune Encephalomyelitis.},
  url          = {http://dx.doi.org/10.1111/j.1365-3083.2006.01866.x},
  volume       = {65},
  year         = {2007},
}