Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of Lewis rats with a single dose of OX19 antibody, specific for rat CD5, uniformly prevented the development of experimental autoimmune encephalomyelitis (EAE). This protective effect had several notable characteristics: (1) it persisted for at least 10 days; (2) it could be achieved with either high doses of the antibody (> 200 micrograms) or lower doses (100-200 micrograms), which did not deplete T cell populations; and (3) the treated animals were able to mount comparable T cell responses to both myelin basic protein and myelin-unrelated antigens. In addition, antibody treatment consistently prevented the development of adoptively transferred EAE, suggesting that enhanced suppressor cell activity may have contributed to the protection. Antibodies such as OX19 appear capable of blocking the development of EAE, and perhaps other autoimmune diseases as well.
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PMID:Prevention of experimental autoimmune encephalomyelitis in Lewis rats by treatment with an anti-rat CD5 antibody (OX19). 128 May 33

Experimental allergic encephalomyelitis (EAE) was induced by adoptive transfer of myelin basic protein (MBP)-activated LEW spleen cells into (LEW x PVG/c) F1----LEW chimeras. By double-immunofluorescent staining using OX27, which is specific for RT1c, and monoclonal antibodies (mAb) against various T-cell antigens (TAg), inflammatory cells in the lesions of the central nervous system (CNS) were categorized into MBP-activated and transferred LEW T cells (TAg+ OX27-), accompanying T cells (TAg+ OX27+) of chimera origin and non-T cells (TAg- OX27+). Examination of the lesions at various stages of EAE revealed that transferred OX19 (CD5)+ T cells accounted for 46% of the total number of inflammatory cells at the preclinical stage, became reduced to 23% at the clinical stage and recovered to a level between those of the preclinical and clinical stages at the recovery stage. In parenchymal infiltrates, 93% of the total T cells were transferred cells at the preclinical stage, whereas 66% were present in perivascular aggregates. At the clinical stage, the proportion of transferred T cells in the parenchyma was not different from that in the perivascular cuffs. At the recovery stage, the proportion of transferred T cells in the parenchyma was increased. Collectively, MBP-activated and transferred T cells first appeared in the CNS parenchyma followed by infiltration of T and non-T cells of recipient (chimera) origin. All these inflammatory cells formed the lesions of full-blown EAE. At the recovery stage, inflammatory cells decreased in number in all the compartments of the CNS. Transferred T cells formed the major proportion of parenchymal infiltrates at this stage. These findings strongly suggest that transferred T cells remain in the CNS parenchyma longer than cells of chimera origin and that antigen-activated T cells have well-expressed CNS-homing activity.
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PMID:Adoptively transferred experimental allergic encephalomyelitis in chimeric rats: identification of transferred cells in the lesions of the central nervous system. 305 24