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Effect of cyclophosphamide pretreatment on autoimmune encephalomyelitis in rats
B. Källén,
M. Dohlsten,
H. Klementsson,
Corresponding Author
B. Källén
Tornblad Institute, University of Lund, Lund, Sweden
Professor Bengt Källén Tornblad Institute Biskopsgatan 7 S-223 62 Lund SwedenSearch for more papers by this authorM. Dohlsten
Tornblad Institute, University of Lund, Lund, Sweden
Search for more papers by this authorH. Klementsson
Tornblad Institute, University of Lund, Lund, Sweden
Search for more papers by this authorB. Källén,
M. Dohlsten,
H. Klementsson,
Corresponding Author
B. Källén
Tornblad Institute, University of Lund, Lund, Sweden
Professor Bengt Källén Tornblad Institute Biskopsgatan 7 S-223 62 Lund SwedenSearch for more papers by this authorM. Dohlsten
Tornblad Institute, University of Lund, Lund, Sweden
Search for more papers by this authorH. Klementsson
Tornblad Institute, University of Lund, Lund, Sweden
Search for more papers by this authorAbstract
We studied the effect of a low dose cyclophosphamide (CY) treatment on the clinical course of experimental autoimmune encephalomyelitis (EAE) in rats from three resistant or low-susceptible strains: Fischer, Brown-Norway, PVG, and the F1 hybrid between the two former strains. Treatment with 40 mg/kg two days before immunization resulted in a marked potentiation of EAE development in Fischer and PVG rats, but not in BN rats or F1(BN x F) hybrids. The effect of the CY treatment was a short period of severe lymphoid cell depletion with an increase in the quotient between T cells reacting with w3/25 monoclonal antiserum and such reacting with ox-8 antiserum, indicating a relative reduction in suppressor/cytotoxic cell counts. Treatment of Fischer or PVG rats, after CY treatment, for five days with thymic hormone factor (THF) normalized T cell ratios and restored the rats to a state of low susceptibility. It is concluded that Fischer and PVG rats have an EAE suppressive mechanism dependent on CY-sensitive suppressor lymphocytes, while there may be other mechanisms of resistance to EAE in BN rats.
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