Ample evidence points to substantial genetic control over aspects of the im
mune response. In essence, all immune systems are not created equally. Sing
le genes with large effects on clinical disease have been documented, yet a
great majority of disease resistance traits are likely to be influenced by
the aggregate of many genes, each with a relatively small effect. Heritabi
lity estimates of immunoresponsiveness traits such as antibody response and
neutrophil function have typically ranged from 0.10 to 0.30. Animal improv
ement programs aimed at enhanced disease resistance in North America will l
ikely use immunoresponsiveness traits as indirect markers for clinical dise
ase resistance.