Abstract

I‐J has been regarded as a polymorphic genetic marker controlled by a locus in the major histocompatibility complex (MHC) which is expressed only on functional T cells. However, this antigenic determinant has been found not to be directly encoded by the MHC gene per se but is somatically generated according to the MHC of the cellular environment during ontogeny. This explains the apparent linkage of I‐J to MHC, despite the failure to find the structural gene for I‐J within the MHC. The I‐J paradox provides an instance of a polymorphism that does not follow the standard genetics of Mendelian structural genes.