Reversal of Experimental Allergic Encephalomyelitis with Monoclonal Antibody to a T-Cell Subset Marker

• Published in: Science (American Association for the Advancement of Science) Vol. 227; no. 4685; pp. 415 - 417
• Main Authors: Waldor, Matthew K., Sriram, Subramanian, Hardy, Richard, Herzenberg, Leonore A., Herzenberg, Leonard A., Lanier, Lewis, Lim, Mae, Steinman, Lawrence
• Format: Journal Article
• Language: English
• Published: Washington, DC The American Association for the Advancement of Science 25-01-1985; American Association for the Advancement of Science
• Subjects: Animals; Antibodies; Antibodies, Monoclonal - therapeutic use; Autoimmune diseases; Autoimmune diseases of the nervous system; Biological and medical sciences; Disease models; Encephalomyelitis, Autoimmune, Experimental - pathology; Encephalomyelitis, Autoimmune, Experimental - therapy; Experimental and animal immunopathology. Animal models; Experimental autoimmune encephalomyelitis; Immunization; Immunopathology; Leukocyte Count; Lymph nodes; Lymph Nodes - pathology; Medical sciences; Mice; Monoclonal antibodies; Multiple sclerosis; Nervous system diseases; Spleen - pathology; T cells; T lymphocytes; T-Lymphocytes, Helper-Inducer - immunology; Vertebrata; Experimental disease; Mammalia; Encephalomyelitis; Mouse; Rodentia; T-Lymphocyte; Autoimmune disease; Monoclonal antibody; Inhibition; Cell subpopulation
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.3155574

Administration of a monoclonal antibody (GK1.5) that recognizes the L3T4 marker present on helper T cells prevented the development of experimental allergic encephalomyelitis (EAE) in mice. Furthermore, treatment with GK1.5 reversed EAE when the antibody was given to paralyzed animals. In vivo injection of GK1.5 selectively reduced the number of L3T4$^{+}$ cells in the spleen and the lymph nodes. These results suggest that manipulation of the human equivalent of the murine L3T4$^{+}$ T-cell subset with monoclonal antibodies may provide effective therapy for certain autoimmune diseases.