Abstract
Recent experimental work in rodents has demonstrated that the liver can function as an ‘IgA—pump’, transporting polymeric IgA from serum to bile via a secretory-component mediated uptake at the surface of the hepatic parenchymal cell. Studies are surveyed which indicate that, although this process occurs in man. it is to a strikingly lesser degree, and interruption of this pathway does not explain the high serum IgA levels often seen in chronic liver disease: the explanation for this lies in enhanced synthesis of IgA, and, diminished polymeric IgA catabolism unrelated to hepatobiliary transport.