Monoclonal Antibody against T-Cell Receptor alphabeta Induces Self-Tolerance in Chronic Experimental Autoimmune Encephalomyelitis.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/165048
- author
- Lavasani, Shahram LU ; Dzhambazov, Balik LU and Andersson, M
- organization
- publishing date
- 2007
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Department of Experimental Medical Science (013210000), Medical Inflammation Research (013212019), Functional Zoology (432112239)
- 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
- 2016-04-01 16:07:49
- date last changed
- 2022-01-28 17:28:15
@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}}, doi = {{10.1111/j.1365-3083.2006.01866.x}}, volume = {{65}}, year = {{2007}}, }