Nature 398, 341— 344 (1999).
It has come to our attention that the conclusions drawn in this paper need to be revised. We have found that the effects attributed to CD30 were the result of background gene(s) of 129 origin. Subsequent backcrossing of the CD30-deficient OT-I line by G. Davey in our laboratory segregated the capacity of low numbers of OT-I cells to cause disease from their capacity to express CD30. Our conclusion that signalling through CD30 protects against autoimmune diabetes must be reconsidered as an effect of a background gene(s) that we are currently mapping.
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