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Overcoming Unresponsiveness in Experimental Autoimmune Encephalomyelitis (EAE) Resistant Mouse Strains by Adoptive Transfer and Antigenic Challenge
Published on: April 9, 2012
Modulation of experimental allergic encephalomyelitis in Lewis rats by monoclonal anti-T cell antibodies
The effect of monoclonal antibodies to different T lymphocyte populations of the rat on the induction and the course of experimental allergic encephalomyelitis (EAE) was investigated. EAE was induced by injection of guinea pig spinal cord in adjuvant. Subcutaneous injections of monoclonal antibodies to all peripheral T lymphocytes (W3/13) abrogated or prevented the development of clinical EAE. Similar results were obtained in animals injected with monoclonal antibodies to T helper cells (W3/25) mixed with monoclonal antibodies to T nonhelper cells (OX8). Animals treated with either W3/25 or OX8 developed clinical EAE as the control rats (subcutaneous injected with normal mouse serum). Histological examination after the acute stage revealed no significant differences between rats treated prophylactically with W3/13, W3/25 or OX8 and rats injected with normal mouse serum. Animals treated prophylactically with a mixture of W3/25 and OX8 developed, on the whole, EAE with less histological severity compared to the control animals. Treatment of rats after the onset of the first clinical symptoms of EAE (tail flaccidity) with W3/13 resulted in a less fatal course of the disease. Compared to surviving rats injected with mouse serum (controls) the number of infiltrates were reduced in these rats treated therapeutically.
The effect of monoclonal antibodies to different T lymphocyte populations of the rat on the induction and the course of experimental allergic encephalomyelitis (EAE) was investigated. EAE was induced by injection of guinea pig spinal cord in adjuvant. Subcutaneous injections of monoclonal antibodies to all peripheral T lymphocytes (W3/13) abrogated or prevented the development of clinical EAE. Similar results were obtained in animals injected with monoclonal antibodies to T helper cells (W3/25) mixed with monoclonal antibodies to T nonhelper cells (OX8). Animals treated with either W3/25 or OX8 developed clinical EAE as the control rats (subcutaneous injected with normal mouse serum). Histological examination after the acute stage revealed no significant differences between rats treated prophylactically with W3/13, W3/25 or OX8 and rats injected with normal mouse serum. Animals treated prophylactically with a mixture of W3/25 and OX8 developed, on the whole, EAE with less histological severity compared to the control animals. Treatment of rats after the onset of the first clinical symptoms of EAE (tail flaccidity) with W3/13 resulted in a less fatal course of the disease. Compared to surviving rats injected with mouse serum (controls) the number of infiltrates were reduced in these rats treated therapeutically.

