A process for inhibiting symptoms of a subject with celiac disease is provided that includes administration of monoclonal-, or polyclonal-, monomeric, dimeric, or polymeric IgA. Joining secretory component to the IgA limits oral administration degradation. Formulating agents are mixed with the monomeric, dimeric, or polymeric IgA to yield a dosing form of a capsule, tablet, and a suppository. The therapeutic is amenable to enrobement directly through microencapsulation or the dosing form is coated with an enteric coating.