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Successful prevention and treatment of autoimmune encephalomyelitis by short-term administration of anti-T-cell receptor alpha beta antibody.
Immunology. 1994 Jan; 81(1):1-7.I

Abstract

To identify an effective immunotherapy for T-cell-mediated autoimmune diseases, prevention and treatment of experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats was attempted by administering a monoclonal antibody (mAb), R73, which is specific for rat T-cell receptor (TcR) alpha beta. Short-term administration of R73 at relatively low doses before immunization with encephalitogenic antigen, myelin basic protein (MBP), prevented the development of EAE. However, treatment with anti-CD4 and anti-Ia mAb in the same protocol was ineffective. Flow cytometric analysis demonstrated that short-term administration of R73 resulted in transient down-regulation of the TcR molecules, whereas the number of CD2-expressing T cells was well preserved. Furthermore, the response to MBP of T cells isolated from rats that were pretreated with R73 and then immunized with MBP was strongly suppressed. On the other hand, the T-cell response of R73-pretreated rats to a third-party antigen which was immunized at a later period was not inhibited. These findings suggest that in vivo administration of a low dose of R73 protects rats from EAE by inducing anergy of MBP-reactive encephalitogenic T cells. Furthermore, R73 treatment which started on day 10 of the immunization (shortly before the day of onset of clinical signs) completely suppressed the induction of EAE and that which started on day 11 (the day of onset) hastened recovery. Since the phenotypes of the TcR V beta chain of encephalitogenic T cells are not so limited as previously believed, immunotherapy with mAb against the TcR alpha beta framework may be one of the best methods for treatment of T-cell-mediated autoimmune diseases.

Authors+Show Affiliations

Department of Immunology, Niigata University School of Medicine, Japan.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

7510661

Citation

Matsumoto, Y, et al. "Successful Prevention and Treatment of Autoimmune Encephalomyelitis By Short-term Administration of anti-T-cell Receptor Alpha Beta Antibody." Immunology, vol. 81, no. 1, 1994, pp. 1-7.
Matsumoto Y, Tsuchida M, Hanawa H, et al. Successful prevention and treatment of autoimmune encephalomyelitis by short-term administration of anti-T-cell receptor alpha beta antibody. Immunology. 1994;81(1):1-7.
Matsumoto, Y., Tsuchida, M., Hanawa, H., & Abo, T. (1994). Successful prevention and treatment of autoimmune encephalomyelitis by short-term administration of anti-T-cell receptor alpha beta antibody. Immunology, 81(1), 1-7.
Matsumoto Y, et al. Successful Prevention and Treatment of Autoimmune Encephalomyelitis By Short-term Administration of anti-T-cell Receptor Alpha Beta Antibody. Immunology. 1994;81(1):1-7. PubMed PMID: 7510661.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Successful prevention and treatment of autoimmune encephalomyelitis by short-term administration of anti-T-cell receptor alpha beta antibody. AU - Matsumoto,Y, AU - Tsuchida,M, AU - Hanawa,H, AU - Abo,T, PY - 1994/1/1/pubmed PY - 1994/1/1/medline PY - 1994/1/1/entrez SP - 1 EP - 7 JF - Immunology JO - Immunology VL - 81 IS - 1 N2 - To identify an effective immunotherapy for T-cell-mediated autoimmune diseases, prevention and treatment of experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats was attempted by administering a monoclonal antibody (mAb), R73, which is specific for rat T-cell receptor (TcR) alpha beta. Short-term administration of R73 at relatively low doses before immunization with encephalitogenic antigen, myelin basic protein (MBP), prevented the development of EAE. However, treatment with anti-CD4 and anti-Ia mAb in the same protocol was ineffective. Flow cytometric analysis demonstrated that short-term administration of R73 resulted in transient down-regulation of the TcR molecules, whereas the number of CD2-expressing T cells was well preserved. Furthermore, the response to MBP of T cells isolated from rats that were pretreated with R73 and then immunized with MBP was strongly suppressed. On the other hand, the T-cell response of R73-pretreated rats to a third-party antigen which was immunized at a later period was not inhibited. These findings suggest that in vivo administration of a low dose of R73 protects rats from EAE by inducing anergy of MBP-reactive encephalitogenic T cells. Furthermore, R73 treatment which started on day 10 of the immunization (shortly before the day of onset of clinical signs) completely suppressed the induction of EAE and that which started on day 11 (the day of onset) hastened recovery. Since the phenotypes of the TcR V beta chain of encephalitogenic T cells are not so limited as previously believed, immunotherapy with mAb against the TcR alpha beta framework may be one of the best methods for treatment of T-cell-mediated autoimmune diseases. SN - 0019-2805 UR - https://www.unboundmedicine.com/medline/citation/7510661/Successful_prevention_and_treatment_of_autoimmune_encephalomyelitis_by_short_term_administration_of_anti_T_cell_receptor_alpha_beta_antibody_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/7510661/ DB - PRIME DP - Unbound Medicine ER -