In most of the higher vertebrates, the majority of IgA is synthesized by gastrointestinal lymphoid tissue, with smaller amounts synthesized at other mucosal sites such as the respiratory tract, salivary glands and reproductive tract. The total quantity of IgA synthesized in humans has been estimated to be 66 mg kg⁻¹ day⁻¹, of which approximately two-thirds is derived from mucosal lymphoid tissue. The relatively large amounts of IgA synthesized daily is concerned with mucosal defense; where the mucosal surfaces are constantly infected with organisms that are either commensal to the host or pathogenic. The bone marrow also provides an additional source of IgA, especially in humans.

IgA has two subclasses; IgA1 and IgA2. Mucosal antigen challenge provokes polymeric IgA (pIgA) production by plasma cells of the mucosa-associated lymphoid tissue. The pIgA is then transported across epithelium into mucosal fluids where it is released after coupling to secretory component as secretory IgA (sIgA), which is bone marrow derived and mostly monomeric IgA1.

IgA is generally increased in skin, pulmonary, kidney infections, IgA nephropathy (Berger’s disease), and hepatic cirrhosis. Increased monoclonal IgA concentrations may be found in multiple myeloma and other disturbances of plasmatic cells.