  We develop a model for speciation due to postzygotic incompatibility
generated by autoimmune reactions. The model is based on predator-prey
interactions between a host plants and their pathogens. Such interactions are
often frequency-dependent, so that pathogen attack is focused on the most
abundant plant phenotype, while rare plant types may escape pathogen attack.
Thus, frequency dependence can generate disruptive selection, which can give
rise to speciation if distant phenotypes become reproductively isolated. Based
on recent experimental evidence from {\it Arabidopsis}, we assume that at the
molecular level, incompatibility between strains is caused by epistatic
interactions between two proteins in the plant immune system, the guard and the
guardee. Within each plant strain, immune reactions occur when the guardee
protein is modified by a pathogen effector, and the guard subsequently binds to
the guardee, thus precipitating an immune response. However, when guard and
guardee proteins come from phenotypically distant parents, a hybrid's immune
system can be triggered by erroneous interactions between these proteins even
in the absence of pathogen attack, leading to severe autoimmune reactions in
hybrids. Our model shows how phenotypic variation generated by
frequency-dependent host-pathogen interactions can lead to postzygotic
incompatibility between extremal types, and hence to speciation.
