Why rethink the structure-function relationships regulating TCR behavior?

Although the generally accepted (Standard) Model of the TCR has powered the accumulation of a large body of crucial data, it is lacking because of the failure of its basic tenet that allele-specific recognition of MHC-encoded restricting elements can be derived by somatic selection on a random repertoire. The limitations of the Standard Model due to this tenet and a glimpse at what a competing model might look like add up to yield a surprising new view of the structure-function relationships of the TCR. A published experiment illustrating this is discussed.